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PMC212319_Fig3_4.jpg | What object or scene is depicted here? | A. Real time image of the translocation of ARF1-GFP to the plasma membrane. HeLa cells that had been stably transfected with ARF1-GFP were transiently transfected with myc-ARNO, serum starved overnight, and treated with 100 nM insulin. Images were collected every 30 seconds using a Molecular Dynamics 2001 confocal microscope. The time intervals that were indicated on the upper right hand corner of each panel represent the time after the addition of insulin. B. The translocation of ARF1-GFP to the plasma membrane by the effects of insulin requires ARNO. ARF1-GFP/HeLa cells were transfected with myc-ARNO, treated, fixed, and stained for myc-epitope as described in the Materials and Methods section. Images displaying ARF1-GFP (green) and myc-ARNO (red) were merged us ing Adobe Photoshop software. |
PMC212319_Fig3_9.jpg | What object or scene is depicted here? | A. Real time image of the translocation of ARF1-GFP to the plasma membrane. HeLa cells that had been stably transfected with ARF1-GFP were transiently transfected with myc-ARNO, serum starved overnight, and treated with 100 nM insulin. Images were collected every 30 seconds using a Molecular Dynamics 2001 confocal microscope. The time intervals that were indicated on the upper right hand corner of each panel represent the time after the addition of insulin. B. The translocation of ARF1-GFP to the plasma membrane by the effects of insulin requires ARNO. ARF1-GFP/HeLa cells were transfected with myc-ARNO, treated, fixed, and stained for myc-epitope as described in the Materials and Methods section. Images displaying ARF1-GFP (green) and myc-ARNO (red) were merged us ing Adobe Photoshop software. |
PMC212319_Fig3_2.jpg | Can you identify the primary element in this image? | A. Real time image of the translocation of ARF1-GFP to the plasma membrane. HeLa cells that had been stably transfected with ARF1-GFP were transiently transfected with myc-ARNO, serum starved overnight, and treated with 100 nM insulin. Images were collected every 30 seconds using a Molecular Dynamics 2001 confocal microscope. The time intervals that were indicated on the upper right hand corner of each panel represent the time after the addition of insulin. B. The translocation of ARF1-GFP to the plasma membrane by the effects of insulin requires ARNO. ARF1-GFP/HeLa cells were transfected with myc-ARNO, treated, fixed, and stained for myc-epitope as described in the Materials and Methods section. Images displaying ARF1-GFP (green) and myc-ARNO (red) were merged us ing Adobe Photoshop software. |
PMC212319_Fig3_1.jpg | What stands out most in this visual? | A. Real time image of the translocation of ARF1-GFP to the plasma membrane. HeLa cells that had been stably transfected with ARF1-GFP were transiently transfected with myc-ARNO, serum starved overnight, and treated with 100 nM insulin. Images were collected every 30 seconds using a Molecular Dynamics 2001 confocal microscope. The time intervals that were indicated on the upper right hand corner of each panel represent the time after the addition of insulin. B. The translocation of ARF1-GFP to the plasma membrane by the effects of insulin requires ARNO. ARF1-GFP/HeLa cells were transfected with myc-ARNO, treated, fixed, and stained for myc-epitope as described in the Materials and Methods section. Images displaying ARF1-GFP (green) and myc-ARNO (red) were merged us ing Adobe Photoshop software. |
PMC212319_Fig3_5.jpg | What does this image primarily show? | A. Real time image of the translocation of ARF1-GFP to the plasma membrane. HeLa cells that had been stably transfected with ARF1-GFP were transiently transfected with myc-ARNO, serum starved overnight, and treated with 100 nM insulin. Images were collected every 30 seconds using a Molecular Dynamics 2001 confocal microscope. The time intervals that were indicated on the upper right hand corner of each panel represent the time after the addition of insulin. B. The translocation of ARF1-GFP to the plasma membrane by the effects of insulin requires ARNO. ARF1-GFP/HeLa cells were transfected with myc-ARNO, treated, fixed, and stained for myc-epitope as described in the Materials and Methods section. Images displaying ARF1-GFP (green) and myc-ARNO (red) were merged us ing Adobe Photoshop software. |
PMC212319_Fig3_7.jpg | What's the most prominent thing you notice in this picture? | A. Real time image of the translocation of ARF1-GFP to the plasma membrane. HeLa cells that had been stably transfected with ARF1-GFP were transiently transfected with myc-ARNO, serum starved overnight, and treated with 100 nM insulin. Images were collected every 30 seconds using a Molecular Dynamics 2001 confocal microscope. The time intervals that were indicated on the upper right hand corner of each panel represent the time after the addition of insulin. B. The translocation of ARF1-GFP to the plasma membrane by the effects of insulin requires ARNO. ARF1-GFP/HeLa cells were transfected with myc-ARNO, treated, fixed, and stained for myc-epitope as described in the Materials and Methods section. Images displaying ARF1-GFP (green) and myc-ARNO (red) were merged us ing Adobe Photoshop software. |
PMC212319_Fig3_3.jpg | What is the main focus of this visual representation? | A. Real time image of the translocation of ARF1-GFP to the plasma membrane. HeLa cells that had been stably transfected with ARF1-GFP were transiently transfected with myc-ARNO, serum starved overnight, and treated with 100 nM insulin. Images were collected every 30 seconds using a Molecular Dynamics 2001 confocal microscope. The time intervals that were indicated on the upper right hand corner of each panel represent the time after the addition of insulin. B. The translocation of ARF1-GFP to the plasma membrane by the effects of insulin requires ARNO. ARF1-GFP/HeLa cells were transfected with myc-ARNO, treated, fixed, and stained for myc-epitope as described in the Materials and Methods section. Images displaying ARF1-GFP (green) and myc-ARNO (red) were merged us ing Adobe Photoshop software. |
PMC212319_Fig3_0.jpg | What is the central feature of this picture? | A. Real time image of the translocation of ARF1-GFP to the plasma membrane. HeLa cells that had been stably transfected with ARF1-GFP were transiently transfected with myc-ARNO, serum starved overnight, and treated with 100 nM insulin. Images were collected every 30 seconds using a Molecular Dynamics 2001 confocal microscope. The time intervals that were indicated on the upper right hand corner of each panel represent the time after the addition of insulin. B. The translocation of ARF1-GFP to the plasma membrane by the effects of insulin requires ARNO. ARF1-GFP/HeLa cells were transfected with myc-ARNO, treated, fixed, and stained for myc-epitope as described in the Materials and Methods section. Images displaying ARF1-GFP (green) and myc-ARNO (red) were merged us ing Adobe Photoshop software. |
PMC212319_Fig3_8.jpg | What key item or scene is captured in this photo? | A. Real time image of the translocation of ARF1-GFP to the plasma membrane. HeLa cells that had been stably transfected with ARF1-GFP were transiently transfected with myc-ARNO, serum starved overnight, and treated with 100 nM insulin. Images were collected every 30 seconds using a Molecular Dynamics 2001 confocal microscope. The time intervals that were indicated on the upper right hand corner of each panel represent the time after the addition of insulin. B. The translocation of ARF1-GFP to the plasma membrane by the effects of insulin requires ARNO. ARF1-GFP/HeLa cells were transfected with myc-ARNO, treated, fixed, and stained for myc-epitope as described in the Materials and Methods section. Images displaying ARF1-GFP (green) and myc-ARNO (red) were merged us ing Adobe Photoshop software. |
PMC212693_pbio-0000014-g001_10.jpg | What is the core subject represented in this visual? | FRAP of HP1–GFP Reveals a Dynamic Association with HeterochromatinA fraction of a heterochromatic cluster (arrowhead) was bleached by a laser pulse, and recovery of fluorescence was monitored by time-lapse imaging. Images were kindly provided by Thierry Cheutin and Tom Misteli. |
PMC212693_pbio-0000014-g001_15.jpg | What is the central feature of this picture? | FRAP of HP1–GFP Reveals a Dynamic Association with HeterochromatinA fraction of a heterochromatic cluster (arrowhead) was bleached by a laser pulse, and recovery of fluorescence was monitored by time-lapse imaging. Images were kindly provided by Thierry Cheutin and Tom Misteli. |
PMC212693_pbio-0000014-g001_13.jpg | What object or scene is depicted here? | FRAP of HP1–GFP Reveals a Dynamic Association with HeterochromatinA fraction of a heterochromatic cluster (arrowhead) was bleached by a laser pulse, and recovery of fluorescence was monitored by time-lapse imaging. Images were kindly provided by Thierry Cheutin and Tom Misteli. |
PMC212699_pbio-0000021-g001_22.jpg | What key item or scene is captured in this photo? | Expression of Three Transcription Factors during Early Bacteriocyte Development(A) Drawings of some stages of pea aphid embryonic development, approximately to scale. Embryos develop viviparously within a follicular epithelium of the ovariole (data not shown). For a complete description, see Miura et al. (2003). Bacteria are transferred at stage 7. Embryos are labeled with bacteria (b), head (h), thoracic (t), and abdominal (a) regions. The three thoracic segments (t1, t2, t2) and germ cells (gc) are indicated in the stage 14 embryo.(B) A drawing of a stage 7 embryo illustrates transovarial transfer of the bacteria (red arrowhead) to the embryo and the presumptive bacteriocyte nuclei (arrow).(C) Confocal micrograph of a stage 6 embryo stained with anti-Dll antibody (red, indicated by arrow). Anti-Dll labels syncytial nuclei (presumptive bacteriocyte nuclei) in the posterior of the embryo.(D) Confocal micrograph of stage 7 embryo stained with anti-Dll and FP6.87 antibodies. Soon after the bacteria begin to invade the embryo, we observe staining with the FP6.87 antibody localized to the nucleoli (blue), which recognizes both Ubx and Abd-A in diverse arthropods, in the same nuclei that are already expressing Dll (red). The region outlined with a broken white box is enlarged in (D′) to show the bacteria, and only the green channel is shown in monochrome. The red arrow indicates one bacterium.(E and F) In these two panels of the same focal plane from the same stage 9 embryo, Ubx/Abd-A staining (blue) is observed throughout the entire nucleus of all nuclei that also express Dll (red).(G) Confocal micrograph of a stage 8 embryo stained with anti-En (yellow). As the transfer of bacteria (arrowhead) is being completed, the bacteriocyte nuclei begin to express En (yellow, indicated with arrow).In (C)–(G), confocal micrographs show only one focal plane of the embryo, so not all bacteriocyte nuclei in each embryo can be seen. In all figures, F-actin is stained with phalloidin (green). Embryos in all figures, except Figure 2, are oriented with anterior of the entire embryo (towards the germarium) to the left. |
PMC212699_pbio-0000021-g001_21.jpg | What does this image primarily show? | Expression of Three Transcription Factors during Early Bacteriocyte Development(A) Drawings of some stages of pea aphid embryonic development, approximately to scale. Embryos develop viviparously within a follicular epithelium of the ovariole (data not shown). For a complete description, see Miura et al. (2003). Bacteria are transferred at stage 7. Embryos are labeled with bacteria (b), head (h), thoracic (t), and abdominal (a) regions. The three thoracic segments (t1, t2, t2) and germ cells (gc) are indicated in the stage 14 embryo.(B) A drawing of a stage 7 embryo illustrates transovarial transfer of the bacteria (red arrowhead) to the embryo and the presumptive bacteriocyte nuclei (arrow).(C) Confocal micrograph of a stage 6 embryo stained with anti-Dll antibody (red, indicated by arrow). Anti-Dll labels syncytial nuclei (presumptive bacteriocyte nuclei) in the posterior of the embryo.(D) Confocal micrograph of stage 7 embryo stained with anti-Dll and FP6.87 antibodies. Soon after the bacteria begin to invade the embryo, we observe staining with the FP6.87 antibody localized to the nucleoli (blue), which recognizes both Ubx and Abd-A in diverse arthropods, in the same nuclei that are already expressing Dll (red). The region outlined with a broken white box is enlarged in (D′) to show the bacteria, and only the green channel is shown in monochrome. The red arrow indicates one bacterium.(E and F) In these two panels of the same focal plane from the same stage 9 embryo, Ubx/Abd-A staining (blue) is observed throughout the entire nucleus of all nuclei that also express Dll (red).(G) Confocal micrograph of a stage 8 embryo stained with anti-En (yellow). As the transfer of bacteria (arrowhead) is being completed, the bacteriocyte nuclei begin to express En (yellow, indicated with arrow).In (C)–(G), confocal micrographs show only one focal plane of the embryo, so not all bacteriocyte nuclei in each embryo can be seen. In all figures, F-actin is stained with phalloidin (green). Embryos in all figures, except Figure 2, are oriented with anterior of the entire embryo (towards the germarium) to the left. |
PMC212699_pbio-0000021-g001_18.jpg | What key item or scene is captured in this photo? | Expression of Three Transcription Factors during Early Bacteriocyte Development(A) Drawings of some stages of pea aphid embryonic development, approximately to scale. Embryos develop viviparously within a follicular epithelium of the ovariole (data not shown). For a complete description, see Miura et al. (2003). Bacteria are transferred at stage 7. Embryos are labeled with bacteria (b), head (h), thoracic (t), and abdominal (a) regions. The three thoracic segments (t1, t2, t2) and germ cells (gc) are indicated in the stage 14 embryo.(B) A drawing of a stage 7 embryo illustrates transovarial transfer of the bacteria (red arrowhead) to the embryo and the presumptive bacteriocyte nuclei (arrow).(C) Confocal micrograph of a stage 6 embryo stained with anti-Dll antibody (red, indicated by arrow). Anti-Dll labels syncytial nuclei (presumptive bacteriocyte nuclei) in the posterior of the embryo.(D) Confocal micrograph of stage 7 embryo stained with anti-Dll and FP6.87 antibodies. Soon after the bacteria begin to invade the embryo, we observe staining with the FP6.87 antibody localized to the nucleoli (blue), which recognizes both Ubx and Abd-A in diverse arthropods, in the same nuclei that are already expressing Dll (red). The region outlined with a broken white box is enlarged in (D′) to show the bacteria, and only the green channel is shown in monochrome. The red arrow indicates one bacterium.(E and F) In these two panels of the same focal plane from the same stage 9 embryo, Ubx/Abd-A staining (blue) is observed throughout the entire nucleus of all nuclei that also express Dll (red).(G) Confocal micrograph of a stage 8 embryo stained with anti-En (yellow). As the transfer of bacteria (arrowhead) is being completed, the bacteriocyte nuclei begin to express En (yellow, indicated with arrow).In (C)–(G), confocal micrographs show only one focal plane of the embryo, so not all bacteriocyte nuclei in each embryo can be seen. In all figures, F-actin is stained with phalloidin (green). Embryos in all figures, except Figure 2, are oriented with anterior of the entire embryo (towards the germarium) to the left. |
PMC212699_pbio-0000021-g001_19.jpg | What object or scene is depicted here? | Expression of Three Transcription Factors during Early Bacteriocyte Development(A) Drawings of some stages of pea aphid embryonic development, approximately to scale. Embryos develop viviparously within a follicular epithelium of the ovariole (data not shown). For a complete description, see Miura et al. (2003). Bacteria are transferred at stage 7. Embryos are labeled with bacteria (b), head (h), thoracic (t), and abdominal (a) regions. The three thoracic segments (t1, t2, t2) and germ cells (gc) are indicated in the stage 14 embryo.(B) A drawing of a stage 7 embryo illustrates transovarial transfer of the bacteria (red arrowhead) to the embryo and the presumptive bacteriocyte nuclei (arrow).(C) Confocal micrograph of a stage 6 embryo stained with anti-Dll antibody (red, indicated by arrow). Anti-Dll labels syncytial nuclei (presumptive bacteriocyte nuclei) in the posterior of the embryo.(D) Confocal micrograph of stage 7 embryo stained with anti-Dll and FP6.87 antibodies. Soon after the bacteria begin to invade the embryo, we observe staining with the FP6.87 antibody localized to the nucleoli (blue), which recognizes both Ubx and Abd-A in diverse arthropods, in the same nuclei that are already expressing Dll (red). The region outlined with a broken white box is enlarged in (D′) to show the bacteria, and only the green channel is shown in monochrome. The red arrow indicates one bacterium.(E and F) In these two panels of the same focal plane from the same stage 9 embryo, Ubx/Abd-A staining (blue) is observed throughout the entire nucleus of all nuclei that also express Dll (red).(G) Confocal micrograph of a stage 8 embryo stained with anti-En (yellow). As the transfer of bacteria (arrowhead) is being completed, the bacteriocyte nuclei begin to express En (yellow, indicated with arrow).In (C)–(G), confocal micrographs show only one focal plane of the embryo, so not all bacteriocyte nuclei in each embryo can be seen. In all figures, F-actin is stained with phalloidin (green). Embryos in all figures, except Figure 2, are oriented with anterior of the entire embryo (towards the germarium) to the left. |
PMC212699_pbio-0000021-g001_17.jpg | What key item or scene is captured in this photo? | Expression of Three Transcription Factors during Early Bacteriocyte Development(A) Drawings of some stages of pea aphid embryonic development, approximately to scale. Embryos develop viviparously within a follicular epithelium of the ovariole (data not shown). For a complete description, see Miura et al. (2003). Bacteria are transferred at stage 7. Embryos are labeled with bacteria (b), head (h), thoracic (t), and abdominal (a) regions. The three thoracic segments (t1, t2, t2) and germ cells (gc) are indicated in the stage 14 embryo.(B) A drawing of a stage 7 embryo illustrates transovarial transfer of the bacteria (red arrowhead) to the embryo and the presumptive bacteriocyte nuclei (arrow).(C) Confocal micrograph of a stage 6 embryo stained with anti-Dll antibody (red, indicated by arrow). Anti-Dll labels syncytial nuclei (presumptive bacteriocyte nuclei) in the posterior of the embryo.(D) Confocal micrograph of stage 7 embryo stained with anti-Dll and FP6.87 antibodies. Soon after the bacteria begin to invade the embryo, we observe staining with the FP6.87 antibody localized to the nucleoli (blue), which recognizes both Ubx and Abd-A in diverse arthropods, in the same nuclei that are already expressing Dll (red). The region outlined with a broken white box is enlarged in (D′) to show the bacteria, and only the green channel is shown in monochrome. The red arrow indicates one bacterium.(E and F) In these two panels of the same focal plane from the same stage 9 embryo, Ubx/Abd-A staining (blue) is observed throughout the entire nucleus of all nuclei that also express Dll (red).(G) Confocal micrograph of a stage 8 embryo stained with anti-En (yellow). As the transfer of bacteria (arrowhead) is being completed, the bacteriocyte nuclei begin to express En (yellow, indicated with arrow).In (C)–(G), confocal micrographs show only one focal plane of the embryo, so not all bacteriocyte nuclei in each embryo can be seen. In all figures, F-actin is stained with phalloidin (green). Embryos in all figures, except Figure 2, are oriented with anterior of the entire embryo (towards the germarium) to the left. |
PMC212699_pbio-0000021-g001_20.jpg | What is being portrayed in this visual content? | Expression of Three Transcription Factors during Early Bacteriocyte Development(A) Drawings of some stages of pea aphid embryonic development, approximately to scale. Embryos develop viviparously within a follicular epithelium of the ovariole (data not shown). For a complete description, see Miura et al. (2003). Bacteria are transferred at stage 7. Embryos are labeled with bacteria (b), head (h), thoracic (t), and abdominal (a) regions. The three thoracic segments (t1, t2, t2) and germ cells (gc) are indicated in the stage 14 embryo.(B) A drawing of a stage 7 embryo illustrates transovarial transfer of the bacteria (red arrowhead) to the embryo and the presumptive bacteriocyte nuclei (arrow).(C) Confocal micrograph of a stage 6 embryo stained with anti-Dll antibody (red, indicated by arrow). Anti-Dll labels syncytial nuclei (presumptive bacteriocyte nuclei) in the posterior of the embryo.(D) Confocal micrograph of stage 7 embryo stained with anti-Dll and FP6.87 antibodies. Soon after the bacteria begin to invade the embryo, we observe staining with the FP6.87 antibody localized to the nucleoli (blue), which recognizes both Ubx and Abd-A in diverse arthropods, in the same nuclei that are already expressing Dll (red). The region outlined with a broken white box is enlarged in (D′) to show the bacteria, and only the green channel is shown in monochrome. The red arrow indicates one bacterium.(E and F) In these two panels of the same focal plane from the same stage 9 embryo, Ubx/Abd-A staining (blue) is observed throughout the entire nucleus of all nuclei that also express Dll (red).(G) Confocal micrograph of a stage 8 embryo stained with anti-En (yellow). As the transfer of bacteria (arrowhead) is being completed, the bacteriocyte nuclei begin to express En (yellow, indicated with arrow).In (C)–(G), confocal micrographs show only one focal plane of the embryo, so not all bacteriocyte nuclei in each embryo can be seen. In all figures, F-actin is stained with phalloidin (green). Embryos in all figures, except Figure 2, are oriented with anterior of the entire embryo (towards the germarium) to the left. |
PMC300883_pbio-0020015-g001_35.jpg | Describe the main subject of this image. | Caspase Activity Is Required for Spermatid Individualization(A–C) Testis of different genotypes were visualized with antibodies specific for activated Drice (green). (A) Wild-type testis. Active DRICE is present in multiple elongated cysts. Cystic bulges (cb) and waste bags (wb) are indicated by arrows. (B and C) Testes from β2tub-DIAP1 and β2tub-p35 males, respectively. Active DRICE is present in elongated cysts, but cystic bulges and waste bags are reduced in number and size.(D–F) Phalloidin-stained investment cones from testes of different genotypes (red). Spermatid axonemes in (D)–(F) are highlighted by the AXO49 antibody, which recognizes polyglycylated β2tub (Bressac et al. 1995) (blue). (D) In wild-type testes, investment cones move as a coordinated group. (E and F) Coordinated investment cone movement is disrupted in cysts from β2tub-DIAP1 and β2tub-p35 males, respectively.(G–L) EM sections of elongated cysts of different genotypes. (G) A cyst from a wild-type male that has undergone individualization. The boxed region is shown at higher magnification in (J), along with the locations of the major mitochondrial derivative (mj), minor mitochondrial derivative (mi), and axoneme (ax). A single spermatid unit is outlined with a dashed line. (H and I) In cysts from β2tub-DIAP1 and β2tub-p35 males, respectively, many spermatid units are present in a common cytoplasm that contains organelles, often including an enlarged minor mitochondrial derivative. Boxed regions of β2tub-DIAP1 and β2tub-p35 cysts shown in (H) and (I) are shown at higher magnification in (K) and (L), respectively. Several examples of multiple spermatids present in a common cytoplasm are outlined by the dashed line in (K) and (L). Scale bar for EM micrographs = 1 μm. |
PMC300883_pbio-0020015-g001_40.jpg | What is being portrayed in this visual content? | Caspase Activity Is Required for Spermatid Individualization(A–C) Testis of different genotypes were visualized with antibodies specific for activated Drice (green). (A) Wild-type testis. Active DRICE is present in multiple elongated cysts. Cystic bulges (cb) and waste bags (wb) are indicated by arrows. (B and C) Testes from β2tub-DIAP1 and β2tub-p35 males, respectively. Active DRICE is present in elongated cysts, but cystic bulges and waste bags are reduced in number and size.(D–F) Phalloidin-stained investment cones from testes of different genotypes (red). Spermatid axonemes in (D)–(F) are highlighted by the AXO49 antibody, which recognizes polyglycylated β2tub (Bressac et al. 1995) (blue). (D) In wild-type testes, investment cones move as a coordinated group. (E and F) Coordinated investment cone movement is disrupted in cysts from β2tub-DIAP1 and β2tub-p35 males, respectively.(G–L) EM sections of elongated cysts of different genotypes. (G) A cyst from a wild-type male that has undergone individualization. The boxed region is shown at higher magnification in (J), along with the locations of the major mitochondrial derivative (mj), minor mitochondrial derivative (mi), and axoneme (ax). A single spermatid unit is outlined with a dashed line. (H and I) In cysts from β2tub-DIAP1 and β2tub-p35 males, respectively, many spermatid units are present in a common cytoplasm that contains organelles, often including an enlarged minor mitochondrial derivative. Boxed regions of β2tub-DIAP1 and β2tub-p35 cysts shown in (H) and (I) are shown at higher magnification in (K) and (L), respectively. Several examples of multiple spermatids present in a common cytoplasm are outlined by the dashed line in (K) and (L). Scale bar for EM micrographs = 1 μm. |
PMC300883_pbio-0020015-g001_36.jpg | Can you identify the primary element in this image? | Caspase Activity Is Required for Spermatid Individualization(A–C) Testis of different genotypes were visualized with antibodies specific for activated Drice (green). (A) Wild-type testis. Active DRICE is present in multiple elongated cysts. Cystic bulges (cb) and waste bags (wb) are indicated by arrows. (B and C) Testes from β2tub-DIAP1 and β2tub-p35 males, respectively. Active DRICE is present in elongated cysts, but cystic bulges and waste bags are reduced in number and size.(D–F) Phalloidin-stained investment cones from testes of different genotypes (red). Spermatid axonemes in (D)–(F) are highlighted by the AXO49 antibody, which recognizes polyglycylated β2tub (Bressac et al. 1995) (blue). (D) In wild-type testes, investment cones move as a coordinated group. (E and F) Coordinated investment cone movement is disrupted in cysts from β2tub-DIAP1 and β2tub-p35 males, respectively.(G–L) EM sections of elongated cysts of different genotypes. (G) A cyst from a wild-type male that has undergone individualization. The boxed region is shown at higher magnification in (J), along with the locations of the major mitochondrial derivative (mj), minor mitochondrial derivative (mi), and axoneme (ax). A single spermatid unit is outlined with a dashed line. (H and I) In cysts from β2tub-DIAP1 and β2tub-p35 males, respectively, many spermatid units are present in a common cytoplasm that contains organelles, often including an enlarged minor mitochondrial derivative. Boxed regions of β2tub-DIAP1 and β2tub-p35 cysts shown in (H) and (I) are shown at higher magnification in (K) and (L), respectively. Several examples of multiple spermatids present in a common cytoplasm are outlined by the dashed line in (K) and (L). Scale bar for EM micrographs = 1 μm. |
PMC300883_pbio-0020015-g001_39.jpg | What object or scene is depicted here? | Caspase Activity Is Required for Spermatid Individualization(A–C) Testis of different genotypes were visualized with antibodies specific for activated Drice (green). (A) Wild-type testis. Active DRICE is present in multiple elongated cysts. Cystic bulges (cb) and waste bags (wb) are indicated by arrows. (B and C) Testes from β2tub-DIAP1 and β2tub-p35 males, respectively. Active DRICE is present in elongated cysts, but cystic bulges and waste bags are reduced in number and size.(D–F) Phalloidin-stained investment cones from testes of different genotypes (red). Spermatid axonemes in (D)–(F) are highlighted by the AXO49 antibody, which recognizes polyglycylated β2tub (Bressac et al. 1995) (blue). (D) In wild-type testes, investment cones move as a coordinated group. (E and F) Coordinated investment cone movement is disrupted in cysts from β2tub-DIAP1 and β2tub-p35 males, respectively.(G–L) EM sections of elongated cysts of different genotypes. (G) A cyst from a wild-type male that has undergone individualization. The boxed region is shown at higher magnification in (J), along with the locations of the major mitochondrial derivative (mj), minor mitochondrial derivative (mi), and axoneme (ax). A single spermatid unit is outlined with a dashed line. (H and I) In cysts from β2tub-DIAP1 and β2tub-p35 males, respectively, many spermatid units are present in a common cytoplasm that contains organelles, often including an enlarged minor mitochondrial derivative. Boxed regions of β2tub-DIAP1 and β2tub-p35 cysts shown in (H) and (I) are shown at higher magnification in (K) and (L), respectively. Several examples of multiple spermatids present in a common cytoplasm are outlined by the dashed line in (K) and (L). Scale bar for EM micrographs = 1 μm. |
PMC300883_pbio-0020015-g001_38.jpg | What is the principal component of this image? | Caspase Activity Is Required for Spermatid Individualization(A–C) Testis of different genotypes were visualized with antibodies specific for activated Drice (green). (A) Wild-type testis. Active DRICE is present in multiple elongated cysts. Cystic bulges (cb) and waste bags (wb) are indicated by arrows. (B and C) Testes from β2tub-DIAP1 and β2tub-p35 males, respectively. Active DRICE is present in elongated cysts, but cystic bulges and waste bags are reduced in number and size.(D–F) Phalloidin-stained investment cones from testes of different genotypes (red). Spermatid axonemes in (D)–(F) are highlighted by the AXO49 antibody, which recognizes polyglycylated β2tub (Bressac et al. 1995) (blue). (D) In wild-type testes, investment cones move as a coordinated group. (E and F) Coordinated investment cone movement is disrupted in cysts from β2tub-DIAP1 and β2tub-p35 males, respectively.(G–L) EM sections of elongated cysts of different genotypes. (G) A cyst from a wild-type male that has undergone individualization. The boxed region is shown at higher magnification in (J), along with the locations of the major mitochondrial derivative (mj), minor mitochondrial derivative (mi), and axoneme (ax). A single spermatid unit is outlined with a dashed line. (H and I) In cysts from β2tub-DIAP1 and β2tub-p35 males, respectively, many spermatid units are present in a common cytoplasm that contains organelles, often including an enlarged minor mitochondrial derivative. Boxed regions of β2tub-DIAP1 and β2tub-p35 cysts shown in (H) and (I) are shown at higher magnification in (K) and (L), respectively. Several examples of multiple spermatids present in a common cytoplasm are outlined by the dashed line in (K) and (L). Scale bar for EM micrographs = 1 μm. |
PMC300883_pbio-0020015-g001_42.jpg | Can you identify the primary element in this image? | Caspase Activity Is Required for Spermatid Individualization(A–C) Testis of different genotypes were visualized with antibodies specific for activated Drice (green). (A) Wild-type testis. Active DRICE is present in multiple elongated cysts. Cystic bulges (cb) and waste bags (wb) are indicated by arrows. (B and C) Testes from β2tub-DIAP1 and β2tub-p35 males, respectively. Active DRICE is present in elongated cysts, but cystic bulges and waste bags are reduced in number and size.(D–F) Phalloidin-stained investment cones from testes of different genotypes (red). Spermatid axonemes in (D)–(F) are highlighted by the AXO49 antibody, which recognizes polyglycylated β2tub (Bressac et al. 1995) (blue). (D) In wild-type testes, investment cones move as a coordinated group. (E and F) Coordinated investment cone movement is disrupted in cysts from β2tub-DIAP1 and β2tub-p35 males, respectively.(G–L) EM sections of elongated cysts of different genotypes. (G) A cyst from a wild-type male that has undergone individualization. The boxed region is shown at higher magnification in (J), along with the locations of the major mitochondrial derivative (mj), minor mitochondrial derivative (mi), and axoneme (ax). A single spermatid unit is outlined with a dashed line. (H and I) In cysts from β2tub-DIAP1 and β2tub-p35 males, respectively, many spermatid units are present in a common cytoplasm that contains organelles, often including an enlarged minor mitochondrial derivative. Boxed regions of β2tub-DIAP1 and β2tub-p35 cysts shown in (H) and (I) are shown at higher magnification in (K) and (L), respectively. Several examples of multiple spermatids present in a common cytoplasm are outlined by the dashed line in (K) and (L). Scale bar for EM micrographs = 1 μm. |
PMC300883_pbio-0020015-g001_34.jpg | What is the focal point of this photograph? | Caspase Activity Is Required for Spermatid Individualization(A–C) Testis of different genotypes were visualized with antibodies specific for activated Drice (green). (A) Wild-type testis. Active DRICE is present in multiple elongated cysts. Cystic bulges (cb) and waste bags (wb) are indicated by arrows. (B and C) Testes from β2tub-DIAP1 and β2tub-p35 males, respectively. Active DRICE is present in elongated cysts, but cystic bulges and waste bags are reduced in number and size.(D–F) Phalloidin-stained investment cones from testes of different genotypes (red). Spermatid axonemes in (D)–(F) are highlighted by the AXO49 antibody, which recognizes polyglycylated β2tub (Bressac et al. 1995) (blue). (D) In wild-type testes, investment cones move as a coordinated group. (E and F) Coordinated investment cone movement is disrupted in cysts from β2tub-DIAP1 and β2tub-p35 males, respectively.(G–L) EM sections of elongated cysts of different genotypes. (G) A cyst from a wild-type male that has undergone individualization. The boxed region is shown at higher magnification in (J), along with the locations of the major mitochondrial derivative (mj), minor mitochondrial derivative (mi), and axoneme (ax). A single spermatid unit is outlined with a dashed line. (H and I) In cysts from β2tub-DIAP1 and β2tub-p35 males, respectively, many spermatid units are present in a common cytoplasm that contains organelles, often including an enlarged minor mitochondrial derivative. Boxed regions of β2tub-DIAP1 and β2tub-p35 cysts shown in (H) and (I) are shown at higher magnification in (K) and (L), respectively. Several examples of multiple spermatids present in a common cytoplasm are outlined by the dashed line in (K) and (L). Scale bar for EM micrographs = 1 μm. |
PMC300883_pbio-0020015-g001_32.jpg | What stands out most in this visual? | Caspase Activity Is Required for Spermatid Individualization(A–C) Testis of different genotypes were visualized with antibodies specific for activated Drice (green). (A) Wild-type testis. Active DRICE is present in multiple elongated cysts. Cystic bulges (cb) and waste bags (wb) are indicated by arrows. (B and C) Testes from β2tub-DIAP1 and β2tub-p35 males, respectively. Active DRICE is present in elongated cysts, but cystic bulges and waste bags are reduced in number and size.(D–F) Phalloidin-stained investment cones from testes of different genotypes (red). Spermatid axonemes in (D)–(F) are highlighted by the AXO49 antibody, which recognizes polyglycylated β2tub (Bressac et al. 1995) (blue). (D) In wild-type testes, investment cones move as a coordinated group. (E and F) Coordinated investment cone movement is disrupted in cysts from β2tub-DIAP1 and β2tub-p35 males, respectively.(G–L) EM sections of elongated cysts of different genotypes. (G) A cyst from a wild-type male that has undergone individualization. The boxed region is shown at higher magnification in (J), along with the locations of the major mitochondrial derivative (mj), minor mitochondrial derivative (mi), and axoneme (ax). A single spermatid unit is outlined with a dashed line. (H and I) In cysts from β2tub-DIAP1 and β2tub-p35 males, respectively, many spermatid units are present in a common cytoplasm that contains organelles, often including an enlarged minor mitochondrial derivative. Boxed regions of β2tub-DIAP1 and β2tub-p35 cysts shown in (H) and (I) are shown at higher magnification in (K) and (L), respectively. Several examples of multiple spermatids present in a common cytoplasm are outlined by the dashed line in (K) and (L). Scale bar for EM micrographs = 1 μm. |
PMC300883_pbio-0020015-g001_33.jpg | What does this image primarily show? | Caspase Activity Is Required for Spermatid Individualization(A–C) Testis of different genotypes were visualized with antibodies specific for activated Drice (green). (A) Wild-type testis. Active DRICE is present in multiple elongated cysts. Cystic bulges (cb) and waste bags (wb) are indicated by arrows. (B and C) Testes from β2tub-DIAP1 and β2tub-p35 males, respectively. Active DRICE is present in elongated cysts, but cystic bulges and waste bags are reduced in number and size.(D–F) Phalloidin-stained investment cones from testes of different genotypes (red). Spermatid axonemes in (D)–(F) are highlighted by the AXO49 antibody, which recognizes polyglycylated β2tub (Bressac et al. 1995) (blue). (D) In wild-type testes, investment cones move as a coordinated group. (E and F) Coordinated investment cone movement is disrupted in cysts from β2tub-DIAP1 and β2tub-p35 males, respectively.(G–L) EM sections of elongated cysts of different genotypes. (G) A cyst from a wild-type male that has undergone individualization. The boxed region is shown at higher magnification in (J), along with the locations of the major mitochondrial derivative (mj), minor mitochondrial derivative (mi), and axoneme (ax). A single spermatid unit is outlined with a dashed line. (H and I) In cysts from β2tub-DIAP1 and β2tub-p35 males, respectively, many spermatid units are present in a common cytoplasm that contains organelles, often including an enlarged minor mitochondrial derivative. Boxed regions of β2tub-DIAP1 and β2tub-p35 cysts shown in (H) and (I) are shown at higher magnification in (K) and (L), respectively. Several examples of multiple spermatids present in a common cytoplasm are outlined by the dashed line in (K) and (L). Scale bar for EM micrographs = 1 μm. |
PMC300883_pbio-0020015-g003_47.jpg | What is the principal component of this image? | DRONC Activation Occurs in Association with Individualization Complexes and Is ARK-Dependent(A and B) Wild-type testis stained for active DRICE (green), phalloidin-stained filamentous actin (red), and TOTO-3-stained DNA (blue). (A) Active DRICE is present throughout the length of cysts undergoing individualization. (B) Higher magnification of the testis in (A). The arrowhead points to a cyst in which the individualization complex has assembled around the spermatid nuclei, but DRICE activation has not occurred. The arrow points to a neighboring cyst in which the individualization complex has just begun to move away from the spermatid nuclei. Active DRICE is now present throughout the length of this cyst, indicating that DRICE activation within a cyst occurs rapidly and globally.(C) Active DRONC (green) is initially present in a punctate pattern, apical to the individualization complex (red) at the base of the testis (arrowheads). The individualization complex then moves through the region containing active DRONC (arrow).(D) Subsequently, active DRONC is found associated with the trailing edge of the individualization complex as it moves apical within the cyst. A higher magnification view of active DRONC staining in the left-most cyst is shown in the inset.(E and F) Active DRONC is eliminated in cysts from β2tub-Ark-RNAi and β2tub-Dn-DRONC testis, respectively. |
PMC300883_pbio-0020015-g003_44.jpg | Can you identify the primary element in this image? | DRONC Activation Occurs in Association with Individualization Complexes and Is ARK-Dependent(A and B) Wild-type testis stained for active DRICE (green), phalloidin-stained filamentous actin (red), and TOTO-3-stained DNA (blue). (A) Active DRICE is present throughout the length of cysts undergoing individualization. (B) Higher magnification of the testis in (A). The arrowhead points to a cyst in which the individualization complex has assembled around the spermatid nuclei, but DRICE activation has not occurred. The arrow points to a neighboring cyst in which the individualization complex has just begun to move away from the spermatid nuclei. Active DRICE is now present throughout the length of this cyst, indicating that DRICE activation within a cyst occurs rapidly and globally.(C) Active DRONC (green) is initially present in a punctate pattern, apical to the individualization complex (red) at the base of the testis (arrowheads). The individualization complex then moves through the region containing active DRONC (arrow).(D) Subsequently, active DRONC is found associated with the trailing edge of the individualization complex as it moves apical within the cyst. A higher magnification view of active DRONC staining in the left-most cyst is shown in the inset.(E and F) Active DRONC is eliminated in cysts from β2tub-Ark-RNAi and β2tub-Dn-DRONC testis, respectively. |
PMC300883_pbio-0020015-g003_49.jpg | Describe the main subject of this image. | DRONC Activation Occurs in Association with Individualization Complexes and Is ARK-Dependent(A and B) Wild-type testis stained for active DRICE (green), phalloidin-stained filamentous actin (red), and TOTO-3-stained DNA (blue). (A) Active DRICE is present throughout the length of cysts undergoing individualization. (B) Higher magnification of the testis in (A). The arrowhead points to a cyst in which the individualization complex has assembled around the spermatid nuclei, but DRICE activation has not occurred. The arrow points to a neighboring cyst in which the individualization complex has just begun to move away from the spermatid nuclei. Active DRICE is now present throughout the length of this cyst, indicating that DRICE activation within a cyst occurs rapidly and globally.(C) Active DRONC (green) is initially present in a punctate pattern, apical to the individualization complex (red) at the base of the testis (arrowheads). The individualization complex then moves through the region containing active DRONC (arrow).(D) Subsequently, active DRONC is found associated with the trailing edge of the individualization complex as it moves apical within the cyst. A higher magnification view of active DRONC staining in the left-most cyst is shown in the inset.(E and F) Active DRONC is eliminated in cysts from β2tub-Ark-RNAi and β2tub-Dn-DRONC testis, respectively. |
PMC300883_pbio-0020015-g006_29.jpg | What key item or scene is captured in this photo? |
driceless Males Lack Active Drice Staining and Show Defects in Individualization(A) Testis from driceless male stained with active DRICE. Active DRICE staining is eliminated.(B) Elongated cysts from driceless male. AXO49 staining (blue) outlines the location of three cystic bulges. Individualization complexes (arrows) are marked with phalloidin (red).(C) Example of a cyst from a driceless male in which individualization has proceeded normally.(D) Example of a cyst from a driceless male in which individualization has failed to occur.(E) Boxed area in (D) shown at higher magnification. A region in which individualization has failed is outlined with a dashed line. |
PMC300883_pbio-0020015-g006_26.jpg | What is the core subject represented in this visual? |
driceless Males Lack Active Drice Staining and Show Defects in Individualization(A) Testis from driceless male stained with active DRICE. Active DRICE staining is eliminated.(B) Elongated cysts from driceless male. AXO49 staining (blue) outlines the location of three cystic bulges. Individualization complexes (arrows) are marked with phalloidin (red).(C) Example of a cyst from a driceless male in which individualization has proceeded normally.(D) Example of a cyst from a driceless male in which individualization has failed to occur.(E) Boxed area in (D) shown at higher magnification. A region in which individualization has failed is outlined with a dashed line. |
PMC300883_pbio-0020015-g006_28.jpg | What object or scene is depicted here? |
driceless Males Lack Active Drice Staining and Show Defects in Individualization(A) Testis from driceless male stained with active DRICE. Active DRICE staining is eliminated.(B) Elongated cysts from driceless male. AXO49 staining (blue) outlines the location of three cystic bulges. Individualization complexes (arrows) are marked with phalloidin (red).(C) Example of a cyst from a driceless male in which individualization has proceeded normally.(D) Example of a cyst from a driceless male in which individualization has failed to occur.(E) Boxed area in (D) shown at higher magnification. A region in which individualization has failed is outlined with a dashed line. |
PMC300883_pbio-0020015-g006_25.jpg | What is the focal point of this photograph? |
driceless Males Lack Active Drice Staining and Show Defects in Individualization(A) Testis from driceless male stained with active DRICE. Active DRICE staining is eliminated.(B) Elongated cysts from driceless male. AXO49 staining (blue) outlines the location of three cystic bulges. Individualization complexes (arrows) are marked with phalloidin (red).(C) Example of a cyst from a driceless male in which individualization has proceeded normally.(D) Example of a cyst from a driceless male in which individualization has failed to occur.(E) Boxed area in (D) shown at higher magnification. A region in which individualization has failed is outlined with a dashed line. |
PMC300883_pbio-0020015-g006_27.jpg | What's the most prominent thing you notice in this picture? |
driceless Males Lack Active Drice Staining and Show Defects in Individualization(A) Testis from driceless male stained with active DRICE. Active DRICE staining is eliminated.(B) Elongated cysts from driceless male. AXO49 staining (blue) outlines the location of three cystic bulges. Individualization complexes (arrows) are marked with phalloidin (red).(C) Example of a cyst from a driceless male in which individualization has proceeded normally.(D) Example of a cyst from a driceless male in which individualization has failed to occur.(E) Boxed area in (D) shown at higher magnification. A region in which individualization has failed is outlined with a dashed line. |
PMC300883_pbio-0020015-g007_30.jpg | What is shown in this image? | Active DRICE Is Eliminated from the Cytoplasm of Wild-Type Spermatids Following Passage of the Individualization Complex, but Not from Spermatids in Which Caspase Activity Has Been Inhibited(A) Cystic bulge from a wild-type cyst stained with active DRICE (red). The cystic bulge (arrowhead) is moving to the left. Active DRICE staining is absent in areas of the spermatid bundle that the individualization complex has passed through and in which excess cytoplasm has been eliminated (arrow).(B) Cystic bulge from a β2tub-p35 cyst. The cystic bulge (arrowhead) is decreased in size, and active DRICE is present in areas of the spermatid bundle through which the individualization complex has moved (arrows). These observations suggest caspase inhibition results in at least a partial failure to eliminate excess cytoplasm, but that this is not necessarily associated with lack of movement of the individualization complex. |
PMC300883_pbio-0020015-g007_31.jpg | What can you see in this picture? | Active DRICE Is Eliminated from the Cytoplasm of Wild-Type Spermatids Following Passage of the Individualization Complex, but Not from Spermatids in Which Caspase Activity Has Been Inhibited(A) Cystic bulge from a wild-type cyst stained with active DRICE (red). The cystic bulge (arrowhead) is moving to the left. Active DRICE staining is absent in areas of the spermatid bundle that the individualization complex has passed through and in which excess cytoplasm has been eliminated (arrow).(B) Cystic bulge from a β2tub-p35 cyst. The cystic bulge (arrowhead) is decreased in size, and active DRICE is present in areas of the spermatid bundle through which the individualization complex has moved (arrows). These observations suggest caspase inhibition results in at least a partial failure to eliminate excess cytoplasm, but that this is not necessarily associated with lack of movement of the individualization complex. |
PMC314300_pbio-0020007-g005_50.jpg | What's the most prominent thing you notice in this picture? | Histological Architecture of CSR Gene Expression in Breast CancerRepresentative ISH of LOXL2 and SDFR1 and IHC of PLOD2, PLAUR, and ESDN are shown (magnification, 200×). Panels for LOXL2, PLAUR, PLOD2, and ESDN represent cores of normal and invasive ductal breast carcinoma from different patients on the same tissue microarray. Panels for SDFR1 demonstrate staining in adjacent normal and carcinoma cells on the same tissue section. Arrows highlight spindle-shaped stromal cells that stain positive for SDFR1 and PLOD2. No signal was detected for the sense probe for ISH or for control IHC without the primary antibody. |
PMC317275_pbio-0020008-g002_74.jpg | What is the central feature of this picture? | Time-Lapse Series of Meiosis Progression in Control, asp, and Colcemid-Treated SpermatocytesTimepoint 0 coincides with the time of NEB revealed by the sudden entry of GFP signal into the nucleus. In control cells (Video 2), microtubules are mainly organised around the centrosomes (arrows). However, when centrosomes are kept away from the nuclear region by mutation in asp (Video 3) or colcemid treatment (Video 4), microtubule nucleation and growth are clearly revealed over the nuclear region (N), well away from the centrosomes. Such noncentrosomal microtubules may form bundles that eventually are sorted into spindlelike bipolar microtubule arrays. Microtubules were labelled with an endogenous GFP–α-tubulin fusion. |
PMC317275_pbio-0020008-g002_65.jpg | What is shown in this image? | Time-Lapse Series of Meiosis Progression in Control, asp, and Colcemid-Treated SpermatocytesTimepoint 0 coincides with the time of NEB revealed by the sudden entry of GFP signal into the nucleus. In control cells (Video 2), microtubules are mainly organised around the centrosomes (arrows). However, when centrosomes are kept away from the nuclear region by mutation in asp (Video 3) or colcemid treatment (Video 4), microtubule nucleation and growth are clearly revealed over the nuclear region (N), well away from the centrosomes. Such noncentrosomal microtubules may form bundles that eventually are sorted into spindlelike bipolar microtubule arrays. Microtubules were labelled with an endogenous GFP–α-tubulin fusion. |
PMC317275_pbio-0020008-g002_73.jpg | What is the focal point of this photograph? | Time-Lapse Series of Meiosis Progression in Control, asp, and Colcemid-Treated SpermatocytesTimepoint 0 coincides with the time of NEB revealed by the sudden entry of GFP signal into the nucleus. In control cells (Video 2), microtubules are mainly organised around the centrosomes (arrows). However, when centrosomes are kept away from the nuclear region by mutation in asp (Video 3) or colcemid treatment (Video 4), microtubule nucleation and growth are clearly revealed over the nuclear region (N), well away from the centrosomes. Such noncentrosomal microtubules may form bundles that eventually are sorted into spindlelike bipolar microtubule arrays. Microtubules were labelled with an endogenous GFP–α-tubulin fusion. |
PMC317275_pbio-0020008-g002_75.jpg | What is the focal point of this photograph? | Time-Lapse Series of Meiosis Progression in Control, asp, and Colcemid-Treated SpermatocytesTimepoint 0 coincides with the time of NEB revealed by the sudden entry of GFP signal into the nucleus. In control cells (Video 2), microtubules are mainly organised around the centrosomes (arrows). However, when centrosomes are kept away from the nuclear region by mutation in asp (Video 3) or colcemid treatment (Video 4), microtubule nucleation and growth are clearly revealed over the nuclear region (N), well away from the centrosomes. Such noncentrosomal microtubules may form bundles that eventually are sorted into spindlelike bipolar microtubule arrays. Microtubules were labelled with an endogenous GFP–α-tubulin fusion. |
PMC317275_pbio-0020008-g002_67.jpg | What is the core subject represented in this visual? | Time-Lapse Series of Meiosis Progression in Control, asp, and Colcemid-Treated SpermatocytesTimepoint 0 coincides with the time of NEB revealed by the sudden entry of GFP signal into the nucleus. In control cells (Video 2), microtubules are mainly organised around the centrosomes (arrows). However, when centrosomes are kept away from the nuclear region by mutation in asp (Video 3) or colcemid treatment (Video 4), microtubule nucleation and growth are clearly revealed over the nuclear region (N), well away from the centrosomes. Such noncentrosomal microtubules may form bundles that eventually are sorted into spindlelike bipolar microtubule arrays. Microtubules were labelled with an endogenous GFP–α-tubulin fusion. |
PMC317275_pbio-0020008-g002_68.jpg | What object or scene is depicted here? | Time-Lapse Series of Meiosis Progression in Control, asp, and Colcemid-Treated SpermatocytesTimepoint 0 coincides with the time of NEB revealed by the sudden entry of GFP signal into the nucleus. In control cells (Video 2), microtubules are mainly organised around the centrosomes (arrows). However, when centrosomes are kept away from the nuclear region by mutation in asp (Video 3) or colcemid treatment (Video 4), microtubule nucleation and growth are clearly revealed over the nuclear region (N), well away from the centrosomes. Such noncentrosomal microtubules may form bundles that eventually are sorted into spindlelike bipolar microtubule arrays. Microtubules were labelled with an endogenous GFP–α-tubulin fusion. |
PMC317275_pbio-0020008-g002_64.jpg | What object or scene is depicted here? | Time-Lapse Series of Meiosis Progression in Control, asp, and Colcemid-Treated SpermatocytesTimepoint 0 coincides with the time of NEB revealed by the sudden entry of GFP signal into the nucleus. In control cells (Video 2), microtubules are mainly organised around the centrosomes (arrows). However, when centrosomes are kept away from the nuclear region by mutation in asp (Video 3) or colcemid treatment (Video 4), microtubule nucleation and growth are clearly revealed over the nuclear region (N), well away from the centrosomes. Such noncentrosomal microtubules may form bundles that eventually are sorted into spindlelike bipolar microtubule arrays. Microtubules were labelled with an endogenous GFP–α-tubulin fusion. |
PMC317275_pbio-0020008-g002_69.jpg | Describe the main subject of this image. | Time-Lapse Series of Meiosis Progression in Control, asp, and Colcemid-Treated SpermatocytesTimepoint 0 coincides with the time of NEB revealed by the sudden entry of GFP signal into the nucleus. In control cells (Video 2), microtubules are mainly organised around the centrosomes (arrows). However, when centrosomes are kept away from the nuclear region by mutation in asp (Video 3) or colcemid treatment (Video 4), microtubule nucleation and growth are clearly revealed over the nuclear region (N), well away from the centrosomes. Such noncentrosomal microtubules may form bundles that eventually are sorted into spindlelike bipolar microtubule arrays. Microtubules were labelled with an endogenous GFP–α-tubulin fusion. |
PMC317275_pbio-0020008-g002_72.jpg | What key item or scene is captured in this photo? | Time-Lapse Series of Meiosis Progression in Control, asp, and Colcemid-Treated SpermatocytesTimepoint 0 coincides with the time of NEB revealed by the sudden entry of GFP signal into the nucleus. In control cells (Video 2), microtubules are mainly organised around the centrosomes (arrows). However, when centrosomes are kept away from the nuclear region by mutation in asp (Video 3) or colcemid treatment (Video 4), microtubule nucleation and growth are clearly revealed over the nuclear region (N), well away from the centrosomes. Such noncentrosomal microtubules may form bundles that eventually are sorted into spindlelike bipolar microtubule arrays. Microtubules were labelled with an endogenous GFP–α-tubulin fusion. |
PMC317275_pbio-0020008-g002_70.jpg | What stands out most in this visual? | Time-Lapse Series of Meiosis Progression in Control, asp, and Colcemid-Treated SpermatocytesTimepoint 0 coincides with the time of NEB revealed by the sudden entry of GFP signal into the nucleus. In control cells (Video 2), microtubules are mainly organised around the centrosomes (arrows). However, when centrosomes are kept away from the nuclear region by mutation in asp (Video 3) or colcemid treatment (Video 4), microtubule nucleation and growth are clearly revealed over the nuclear region (N), well away from the centrosomes. Such noncentrosomal microtubules may form bundles that eventually are sorted into spindlelike bipolar microtubule arrays. Microtubules were labelled with an endogenous GFP–α-tubulin fusion. |
PMC317275_pbio-0020008-g002_63.jpg | What does this image primarily show? | Time-Lapse Series of Meiosis Progression in Control, asp, and Colcemid-Treated SpermatocytesTimepoint 0 coincides with the time of NEB revealed by the sudden entry of GFP signal into the nucleus. In control cells (Video 2), microtubules are mainly organised around the centrosomes (arrows). However, when centrosomes are kept away from the nuclear region by mutation in asp (Video 3) or colcemid treatment (Video 4), microtubule nucleation and growth are clearly revealed over the nuclear region (N), well away from the centrosomes. Such noncentrosomal microtubules may form bundles that eventually are sorted into spindlelike bipolar microtubule arrays. Microtubules were labelled with an endogenous GFP–α-tubulin fusion. |
PMC317275_pbio-0020008-g002_76.jpg | What is the dominant medical problem in this image? | Time-Lapse Series of Meiosis Progression in Control, asp, and Colcemid-Treated SpermatocytesTimepoint 0 coincides with the time of NEB revealed by the sudden entry of GFP signal into the nucleus. In control cells (Video 2), microtubules are mainly organised around the centrosomes (arrows). However, when centrosomes are kept away from the nuclear region by mutation in asp (Video 3) or colcemid treatment (Video 4), microtubule nucleation and growth are clearly revealed over the nuclear region (N), well away from the centrosomes. Such noncentrosomal microtubules may form bundles that eventually are sorted into spindlelike bipolar microtubule arrays. Microtubules were labelled with an endogenous GFP–α-tubulin fusion. |
PMC317275_pbio-0020008-g004_59.jpg | What's the most prominent thing you notice in this picture? | The Place of Noncentrosomal Microtubule NucleationThe initial stages of noncentrosomal microtubule nucleation revealed by an endogenous GFP–α-tubulin fusion (left) and phase contrast (right). Following the corresponding videos, it is possible to unmistakably tell the chromosomes (arrows) apart form the other phase-dark objects that are present over the nuclear region (asterisks). The cell in (A) is shown as a single timeframe and the cell in (B) as a time-lapse series. In both cells, noncentrosomal microtubule nucleation (arrowheads) takes place close to the remains on the NE and does not overlap with the major chromosomes. Nucleation sites can be clustered (A) or dispersed (B). In the time-lapse series (B), only the chromosomes that are in focus are labelled. Timepoint 0 min in these series corresponds to the first sign of noncentrosomal microtubule nucleation, around 11 min after NEB. A white bar marks the growing end of a microtubule bundle that at timepoint 93 min reaches one of the bivalents. |
PMC317275_pbio-0020008-g004_52.jpg | What is the focal point of this photograph? | The Place of Noncentrosomal Microtubule NucleationThe initial stages of noncentrosomal microtubule nucleation revealed by an endogenous GFP–α-tubulin fusion (left) and phase contrast (right). Following the corresponding videos, it is possible to unmistakably tell the chromosomes (arrows) apart form the other phase-dark objects that are present over the nuclear region (asterisks). The cell in (A) is shown as a single timeframe and the cell in (B) as a time-lapse series. In both cells, noncentrosomal microtubule nucleation (arrowheads) takes place close to the remains on the NE and does not overlap with the major chromosomes. Nucleation sites can be clustered (A) or dispersed (B). In the time-lapse series (B), only the chromosomes that are in focus are labelled. Timepoint 0 min in these series corresponds to the first sign of noncentrosomal microtubule nucleation, around 11 min after NEB. A white bar marks the growing end of a microtubule bundle that at timepoint 93 min reaches one of the bivalents. |
PMC317275_pbio-0020008-g004_60.jpg | Can you identify the primary element in this image? | The Place of Noncentrosomal Microtubule NucleationThe initial stages of noncentrosomal microtubule nucleation revealed by an endogenous GFP–α-tubulin fusion (left) and phase contrast (right). Following the corresponding videos, it is possible to unmistakably tell the chromosomes (arrows) apart form the other phase-dark objects that are present over the nuclear region (asterisks). The cell in (A) is shown as a single timeframe and the cell in (B) as a time-lapse series. In both cells, noncentrosomal microtubule nucleation (arrowheads) takes place close to the remains on the NE and does not overlap with the major chromosomes. Nucleation sites can be clustered (A) or dispersed (B). In the time-lapse series (B), only the chromosomes that are in focus are labelled. Timepoint 0 min in these series corresponds to the first sign of noncentrosomal microtubule nucleation, around 11 min after NEB. A white bar marks the growing end of a microtubule bundle that at timepoint 93 min reaches one of the bivalents. |
PMC317275_pbio-0020008-g004_55.jpg | What key item or scene is captured in this photo? | The Place of Noncentrosomal Microtubule NucleationThe initial stages of noncentrosomal microtubule nucleation revealed by an endogenous GFP–α-tubulin fusion (left) and phase contrast (right). Following the corresponding videos, it is possible to unmistakably tell the chromosomes (arrows) apart form the other phase-dark objects that are present over the nuclear region (asterisks). The cell in (A) is shown as a single timeframe and the cell in (B) as a time-lapse series. In both cells, noncentrosomal microtubule nucleation (arrowheads) takes place close to the remains on the NE and does not overlap with the major chromosomes. Nucleation sites can be clustered (A) or dispersed (B). In the time-lapse series (B), only the chromosomes that are in focus are labelled. Timepoint 0 min in these series corresponds to the first sign of noncentrosomal microtubule nucleation, around 11 min after NEB. A white bar marks the growing end of a microtubule bundle that at timepoint 93 min reaches one of the bivalents. |
PMC317275_pbio-0020008-g004_58.jpg | What is the dominant medical problem in this image? | The Place of Noncentrosomal Microtubule NucleationThe initial stages of noncentrosomal microtubule nucleation revealed by an endogenous GFP–α-tubulin fusion (left) and phase contrast (right). Following the corresponding videos, it is possible to unmistakably tell the chromosomes (arrows) apart form the other phase-dark objects that are present over the nuclear region (asterisks). The cell in (A) is shown as a single timeframe and the cell in (B) as a time-lapse series. In both cells, noncentrosomal microtubule nucleation (arrowheads) takes place close to the remains on the NE and does not overlap with the major chromosomes. Nucleation sites can be clustered (A) or dispersed (B). In the time-lapse series (B), only the chromosomes that are in focus are labelled. Timepoint 0 min in these series corresponds to the first sign of noncentrosomal microtubule nucleation, around 11 min after NEB. A white bar marks the growing end of a microtubule bundle that at timepoint 93 min reaches one of the bivalents. |
PMC317275_pbio-0020008-g004_53.jpg | What's the most prominent thing you notice in this picture? | The Place of Noncentrosomal Microtubule NucleationThe initial stages of noncentrosomal microtubule nucleation revealed by an endogenous GFP–α-tubulin fusion (left) and phase contrast (right). Following the corresponding videos, it is possible to unmistakably tell the chromosomes (arrows) apart form the other phase-dark objects that are present over the nuclear region (asterisks). The cell in (A) is shown as a single timeframe and the cell in (B) as a time-lapse series. In both cells, noncentrosomal microtubule nucleation (arrowheads) takes place close to the remains on the NE and does not overlap with the major chromosomes. Nucleation sites can be clustered (A) or dispersed (B). In the time-lapse series (B), only the chromosomes that are in focus are labelled. Timepoint 0 min in these series corresponds to the first sign of noncentrosomal microtubule nucleation, around 11 min after NEB. A white bar marks the growing end of a microtubule bundle that at timepoint 93 min reaches one of the bivalents. |
PMC317275_pbio-0020008-g004_57.jpg | What is the core subject represented in this visual? | The Place of Noncentrosomal Microtubule NucleationThe initial stages of noncentrosomal microtubule nucleation revealed by an endogenous GFP–α-tubulin fusion (left) and phase contrast (right). Following the corresponding videos, it is possible to unmistakably tell the chromosomes (arrows) apart form the other phase-dark objects that are present over the nuclear region (asterisks). The cell in (A) is shown as a single timeframe and the cell in (B) as a time-lapse series. In both cells, noncentrosomal microtubule nucleation (arrowheads) takes place close to the remains on the NE and does not overlap with the major chromosomes. Nucleation sites can be clustered (A) or dispersed (B). In the time-lapse series (B), only the chromosomes that are in focus are labelled. Timepoint 0 min in these series corresponds to the first sign of noncentrosomal microtubule nucleation, around 11 min after NEB. A white bar marks the growing end of a microtubule bundle that at timepoint 93 min reaches one of the bivalents. |
PMC317275_pbio-0020008-g004_54.jpg | What is the principal component of this image? | The Place of Noncentrosomal Microtubule NucleationThe initial stages of noncentrosomal microtubule nucleation revealed by an endogenous GFP–α-tubulin fusion (left) and phase contrast (right). Following the corresponding videos, it is possible to unmistakably tell the chromosomes (arrows) apart form the other phase-dark objects that are present over the nuclear region (asterisks). The cell in (A) is shown as a single timeframe and the cell in (B) as a time-lapse series. In both cells, noncentrosomal microtubule nucleation (arrowheads) takes place close to the remains on the NE and does not overlap with the major chromosomes. Nucleation sites can be clustered (A) or dispersed (B). In the time-lapse series (B), only the chromosomes that are in focus are labelled. Timepoint 0 min in these series corresponds to the first sign of noncentrosomal microtubule nucleation, around 11 min after NEB. A white bar marks the growing end of a microtubule bundle that at timepoint 93 min reaches one of the bivalents. |
PMC317275_pbio-0020008-g004_56.jpg | What is being portrayed in this visual content? | The Place of Noncentrosomal Microtubule NucleationThe initial stages of noncentrosomal microtubule nucleation revealed by an endogenous GFP–α-tubulin fusion (left) and phase contrast (right). Following the corresponding videos, it is possible to unmistakably tell the chromosomes (arrows) apart form the other phase-dark objects that are present over the nuclear region (asterisks). The cell in (A) is shown as a single timeframe and the cell in (B) as a time-lapse series. In both cells, noncentrosomal microtubule nucleation (arrowheads) takes place close to the remains on the NE and does not overlap with the major chromosomes. Nucleation sites can be clustered (A) or dispersed (B). In the time-lapse series (B), only the chromosomes that are in focus are labelled. Timepoint 0 min in these series corresponds to the first sign of noncentrosomal microtubule nucleation, around 11 min after NEB. A white bar marks the growing end of a microtubule bundle that at timepoint 93 min reaches one of the bivalents. |
PMC317275_pbio-0020008-g004_61.jpg | What is the dominant medical problem in this image? | The Place of Noncentrosomal Microtubule NucleationThe initial stages of noncentrosomal microtubule nucleation revealed by an endogenous GFP–α-tubulin fusion (left) and phase contrast (right). Following the corresponding videos, it is possible to unmistakably tell the chromosomes (arrows) apart form the other phase-dark objects that are present over the nuclear region (asterisks). The cell in (A) is shown as a single timeframe and the cell in (B) as a time-lapse series. In both cells, noncentrosomal microtubule nucleation (arrowheads) takes place close to the remains on the NE and does not overlap with the major chromosomes. Nucleation sites can be clustered (A) or dispersed (B). In the time-lapse series (B), only the chromosomes that are in focus are labelled. Timepoint 0 min in these series corresponds to the first sign of noncentrosomal microtubule nucleation, around 11 min after NEB. A white bar marks the growing end of a microtubule bundle that at timepoint 93 min reaches one of the bivalents. |
PMC317275_pbio-0020008-g006_79.jpg | What is being portrayed in this visual content? | Correlation between the Orientation of the Cytokinesis Furrow, the Asters, and the Spindle in asp SpermatocytesSchematic representation (A–C) of the relative position of the asters (red), the spindle (yellow), and the cytokinesis furrow (blue), corresponding to a control cell (D) and two examples of asp mutant spermatocytes (E and F), respectively. Asters (arrows) and spindles are labelled with a GFP–α-tubulin fusion. The position of the cleavage furrow (double-headed arrow) was determined by time-lapse imaging of these cells (data not shown). In wild-type cells (n = 10), plotting spindle and furrow orientation relative to the interastral axes shows that asters and spindle are tightly aligned, and cleavage occurs at an angle of 90° ± 10° with respect to them (G). In asp spermatocytes (n = 10), the plane of cleavage occurs at a 90° ± 10° angle with respect to the asters and does not correlate with the orientation of the anastral spindle. |
PMC317275_pbio-0020008-g006_78.jpg | What is the core subject represented in this visual? | Correlation between the Orientation of the Cytokinesis Furrow, the Asters, and the Spindle in asp SpermatocytesSchematic representation (A–C) of the relative position of the asters (red), the spindle (yellow), and the cytokinesis furrow (blue), corresponding to a control cell (D) and two examples of asp mutant spermatocytes (E and F), respectively. Asters (arrows) and spindles are labelled with a GFP–α-tubulin fusion. The position of the cleavage furrow (double-headed arrow) was determined by time-lapse imaging of these cells (data not shown). In wild-type cells (n = 10), plotting spindle and furrow orientation relative to the interastral axes shows that asters and spindle are tightly aligned, and cleavage occurs at an angle of 90° ± 10° with respect to them (G). In asp spermatocytes (n = 10), the plane of cleavage occurs at a 90° ± 10° angle with respect to the asters and does not correlate with the orientation of the anastral spindle. |
PMC340949_pbio-0020046-g003_87.jpg | Describe the main subject of this image. | Decreased Fiber CoherenceDecreased fiber coherences, as observed with DTI, in persistent developmental stutterers compared with a fluent control group. A red dot indicates the peak difference in a coronal (top left), axial (top right), and a sagittal (bottom) slice. |
PMC340949_pbio-0020046-g003_86.jpg | What can you see in this picture? | Decreased Fiber CoherenceDecreased fiber coherences, as observed with DTI, in persistent developmental stutterers compared with a fluent control group. A red dot indicates the peak difference in a coronal (top left), axial (top right), and a sagittal (bottom) slice. |
PMC340949_pbio-0020046-g003_85.jpg | What's the most prominent thing you notice in this picture? | Decreased Fiber CoherenceDecreased fiber coherences, as observed with DTI, in persistent developmental stutterers compared with a fluent control group. A red dot indicates the peak difference in a coronal (top left), axial (top right), and a sagittal (bottom) slice. |
PMC340949_pbio-0020046-g003_89.jpg | What does this image primarily show? | Decreased Fiber CoherenceDecreased fiber coherences, as observed with DTI, in persistent developmental stutterers compared with a fluent control group. A red dot indicates the peak difference in a coronal (top left), axial (top right), and a sagittal (bottom) slice. |
PMC387268_pbio-0020097-g002_93.jpg | What is the focal point of this photograph? | FMRI Insight Effect in RH aSTG(A) Voxels showing greater FMRI signal for insight than noninsight solutions, overlaid on the averaged normalized structural image of all subjects. The active area has a volume of 531 mm3 (peak t = 4.89 at 44, −9, −9 in Talairach space).(B) and (C) Group average signal change following the solution event, for insight (red line) and noninsight (blue line) solutions (yellow arrow indicates button press): (B) over entire LH aSTG region; (C) over entire RH aSTG region.(D) Insight solution signal change minus noninsight solution signal change, in RH aSTG (error bars show the standard error of the mean of the difference at each timepoint). |
PMC387268_pbio-0020097-g002_94.jpg | What key item or scene is captured in this photo? | FMRI Insight Effect in RH aSTG(A) Voxels showing greater FMRI signal for insight than noninsight solutions, overlaid on the averaged normalized structural image of all subjects. The active area has a volume of 531 mm3 (peak t = 4.89 at 44, −9, −9 in Talairach space).(B) and (C) Group average signal change following the solution event, for insight (red line) and noninsight (blue line) solutions (yellow arrow indicates button press): (B) over entire LH aSTG region; (C) over entire RH aSTG region.(D) Insight solution signal change minus noninsight solution signal change, in RH aSTG (error bars show the standard error of the mean of the difference at each timepoint). |
PMC387268_pbio-0020097-g003_96.jpg | What does this image primarily show? | FMRI Signal in RH aSTG during Initial Solving Efforts(A) Voxels in right temporal lobe showing baseline-to-peak event-related FMRI signal when subjects first encounter problems, overlaid on the averaged normalized structural image of all subjects. The cluster is in RH aSTG, with a volume of 469 mm3, with peak t value of 4.37 at 41, −6, −12 in Talairach space, clearly overlapping with the cluster showing an insight effect at solution.(B) Group average signal change following problem onset (time = 0), for the cluster defined by signal at the problem onset (green line) and the cluster (illustrated in Figure 2A) showing the insight effect at solution (white line). Error bars show the standard error of the mean of the difference at each time point. |
PMC406391_pbio-0020129-g001_109.jpg | What stands out most in this visual? | Embryos with Defective Myocardial Function Do Not Form AV ECs(A–C) Fluorescence micrographs of embryos carrying a tie2::GFP transgene, visualized at 48 hpf. In (A), the endocardial ring is visible as a collection of GFP-positive cells at the AV boundary in wild-type (wt) embryos (red arrow). In (B), sih−/− embryos fail to form an AV ring at 48 hpf. In (C), cfk−/− embryos fail to form an AV ring at 48 hpf.(D and E) Cushion development remains defective in cfk−/− embryos. In (D), a 5 μm hematoxylin and eosin-stained plastic section shows the initial stages of cushion development at the AV boundary (red arrows) in a 72 hpf wild-type embryo, with the ECs being two to three cell layers thick at this stage. In (E), a cfk
−/− embryo at 72 hpf shows dilation of both chambers of a blood-filled heart with no evidence of cushion formation at the AV boundary (red arrows).(F and G) cfk−/− embryos fail to form ECs at late stages. Embryos were visualized at identical magnification after counter-staining with rhodamine phalloidin. Red blood cells (RBCs) are seen in the atria of the hearts. In (F), confocal microscopy of a 96 hpf wild-type heart from a tie2::GFP line shows triangular ECs at the AV boundary (blue arrows). In (G), cfk−/− embryos at 96 hpf lack cushion formation and clustering of GFP-positive cells at the AV boundary (blue arrows).(H) At 72 hpf, wild-type embryos have narrow hearts with forward blood flow through the embryo.(I) At 72 hpf, cfk−/− embryos have dilated hearts filled with blood that regurgitates freely from the ventricle to the atrium.(J and K) The initial phenotype in cfk−/− embryos is cardiac dilation at 36 hpf. In (J), wild-type embryos have a narrow ventricle and generate pulsatile flow at 36 hpf. In (K), cfk−/− embryos have an increased end-diastolic diameter (on average 1.18× wild-type, p < 0.01) and do not generate blood flow at 36 hpf.(L and M) Increased bmp-4 expression at the AV boundary (red arrow) is observed in wild-type (L) and cfk−/− (M) embryos at 42 hpf in anticipation of endocardial ring formation.(N) Orientation of the embryos shown in (L) and (M). |
PMC406391_pbio-0020129-g001_106.jpg | What is shown in this image? | Embryos with Defective Myocardial Function Do Not Form AV ECs(A–C) Fluorescence micrographs of embryos carrying a tie2::GFP transgene, visualized at 48 hpf. In (A), the endocardial ring is visible as a collection of GFP-positive cells at the AV boundary in wild-type (wt) embryos (red arrow). In (B), sih−/− embryos fail to form an AV ring at 48 hpf. In (C), cfk−/− embryos fail to form an AV ring at 48 hpf.(D and E) Cushion development remains defective in cfk−/− embryos. In (D), a 5 μm hematoxylin and eosin-stained plastic section shows the initial stages of cushion development at the AV boundary (red arrows) in a 72 hpf wild-type embryo, with the ECs being two to three cell layers thick at this stage. In (E), a cfk
−/− embryo at 72 hpf shows dilation of both chambers of a blood-filled heart with no evidence of cushion formation at the AV boundary (red arrows).(F and G) cfk−/− embryos fail to form ECs at late stages. Embryos were visualized at identical magnification after counter-staining with rhodamine phalloidin. Red blood cells (RBCs) are seen in the atria of the hearts. In (F), confocal microscopy of a 96 hpf wild-type heart from a tie2::GFP line shows triangular ECs at the AV boundary (blue arrows). In (G), cfk−/− embryos at 96 hpf lack cushion formation and clustering of GFP-positive cells at the AV boundary (blue arrows).(H) At 72 hpf, wild-type embryos have narrow hearts with forward blood flow through the embryo.(I) At 72 hpf, cfk−/− embryos have dilated hearts filled with blood that regurgitates freely from the ventricle to the atrium.(J and K) The initial phenotype in cfk−/− embryos is cardiac dilation at 36 hpf. In (J), wild-type embryos have a narrow ventricle and generate pulsatile flow at 36 hpf. In (K), cfk−/− embryos have an increased end-diastolic diameter (on average 1.18× wild-type, p < 0.01) and do not generate blood flow at 36 hpf.(L and M) Increased bmp-4 expression at the AV boundary (red arrow) is observed in wild-type (L) and cfk−/− (M) embryos at 42 hpf in anticipation of endocardial ring formation.(N) Orientation of the embryos shown in (L) and (M). |
PMC406391_pbio-0020129-g001_108.jpg | What object or scene is depicted here? | Embryos with Defective Myocardial Function Do Not Form AV ECs(A–C) Fluorescence micrographs of embryos carrying a tie2::GFP transgene, visualized at 48 hpf. In (A), the endocardial ring is visible as a collection of GFP-positive cells at the AV boundary in wild-type (wt) embryos (red arrow). In (B), sih−/− embryos fail to form an AV ring at 48 hpf. In (C), cfk−/− embryos fail to form an AV ring at 48 hpf.(D and E) Cushion development remains defective in cfk−/− embryos. In (D), a 5 μm hematoxylin and eosin-stained plastic section shows the initial stages of cushion development at the AV boundary (red arrows) in a 72 hpf wild-type embryo, with the ECs being two to three cell layers thick at this stage. In (E), a cfk
−/− embryo at 72 hpf shows dilation of both chambers of a blood-filled heart with no evidence of cushion formation at the AV boundary (red arrows).(F and G) cfk−/− embryos fail to form ECs at late stages. Embryos were visualized at identical magnification after counter-staining with rhodamine phalloidin. Red blood cells (RBCs) are seen in the atria of the hearts. In (F), confocal microscopy of a 96 hpf wild-type heart from a tie2::GFP line shows triangular ECs at the AV boundary (blue arrows). In (G), cfk−/− embryos at 96 hpf lack cushion formation and clustering of GFP-positive cells at the AV boundary (blue arrows).(H) At 72 hpf, wild-type embryos have narrow hearts with forward blood flow through the embryo.(I) At 72 hpf, cfk−/− embryos have dilated hearts filled with blood that regurgitates freely from the ventricle to the atrium.(J and K) The initial phenotype in cfk−/− embryos is cardiac dilation at 36 hpf. In (J), wild-type embryos have a narrow ventricle and generate pulsatile flow at 36 hpf. In (K), cfk−/− embryos have an increased end-diastolic diameter (on average 1.18× wild-type, p < 0.01) and do not generate blood flow at 36 hpf.(L and M) Increased bmp-4 expression at the AV boundary (red arrow) is observed in wild-type (L) and cfk−/− (M) embryos at 42 hpf in anticipation of endocardial ring formation.(N) Orientation of the embryos shown in (L) and (M). |
PMC406391_pbio-0020129-g001_99.jpg | What is the central feature of this picture? | Embryos with Defective Myocardial Function Do Not Form AV ECs(A–C) Fluorescence micrographs of embryos carrying a tie2::GFP transgene, visualized at 48 hpf. In (A), the endocardial ring is visible as a collection of GFP-positive cells at the AV boundary in wild-type (wt) embryos (red arrow). In (B), sih−/− embryos fail to form an AV ring at 48 hpf. In (C), cfk−/− embryos fail to form an AV ring at 48 hpf.(D and E) Cushion development remains defective in cfk−/− embryos. In (D), a 5 μm hematoxylin and eosin-stained plastic section shows the initial stages of cushion development at the AV boundary (red arrows) in a 72 hpf wild-type embryo, with the ECs being two to three cell layers thick at this stage. In (E), a cfk
−/− embryo at 72 hpf shows dilation of both chambers of a blood-filled heart with no evidence of cushion formation at the AV boundary (red arrows).(F and G) cfk−/− embryos fail to form ECs at late stages. Embryos were visualized at identical magnification after counter-staining with rhodamine phalloidin. Red blood cells (RBCs) are seen in the atria of the hearts. In (F), confocal microscopy of a 96 hpf wild-type heart from a tie2::GFP line shows triangular ECs at the AV boundary (blue arrows). In (G), cfk−/− embryos at 96 hpf lack cushion formation and clustering of GFP-positive cells at the AV boundary (blue arrows).(H) At 72 hpf, wild-type embryos have narrow hearts with forward blood flow through the embryo.(I) At 72 hpf, cfk−/− embryos have dilated hearts filled with blood that regurgitates freely from the ventricle to the atrium.(J and K) The initial phenotype in cfk−/− embryos is cardiac dilation at 36 hpf. In (J), wild-type embryos have a narrow ventricle and generate pulsatile flow at 36 hpf. In (K), cfk−/− embryos have an increased end-diastolic diameter (on average 1.18× wild-type, p < 0.01) and do not generate blood flow at 36 hpf.(L and M) Increased bmp-4 expression at the AV boundary (red arrow) is observed in wild-type (L) and cfk−/− (M) embryos at 42 hpf in anticipation of endocardial ring formation.(N) Orientation of the embryos shown in (L) and (M). |
PMC406391_pbio-0020129-g001_107.jpg | What key item or scene is captured in this photo? | Embryos with Defective Myocardial Function Do Not Form AV ECs(A–C) Fluorescence micrographs of embryos carrying a tie2::GFP transgene, visualized at 48 hpf. In (A), the endocardial ring is visible as a collection of GFP-positive cells at the AV boundary in wild-type (wt) embryos (red arrow). In (B), sih−/− embryos fail to form an AV ring at 48 hpf. In (C), cfk−/− embryos fail to form an AV ring at 48 hpf.(D and E) Cushion development remains defective in cfk−/− embryos. In (D), a 5 μm hematoxylin and eosin-stained plastic section shows the initial stages of cushion development at the AV boundary (red arrows) in a 72 hpf wild-type embryo, with the ECs being two to three cell layers thick at this stage. In (E), a cfk
−/− embryo at 72 hpf shows dilation of both chambers of a blood-filled heart with no evidence of cushion formation at the AV boundary (red arrows).(F and G) cfk−/− embryos fail to form ECs at late stages. Embryos were visualized at identical magnification after counter-staining with rhodamine phalloidin. Red blood cells (RBCs) are seen in the atria of the hearts. In (F), confocal microscopy of a 96 hpf wild-type heart from a tie2::GFP line shows triangular ECs at the AV boundary (blue arrows). In (G), cfk−/− embryos at 96 hpf lack cushion formation and clustering of GFP-positive cells at the AV boundary (blue arrows).(H) At 72 hpf, wild-type embryos have narrow hearts with forward blood flow through the embryo.(I) At 72 hpf, cfk−/− embryos have dilated hearts filled with blood that regurgitates freely from the ventricle to the atrium.(J and K) The initial phenotype in cfk−/− embryos is cardiac dilation at 36 hpf. In (J), wild-type embryos have a narrow ventricle and generate pulsatile flow at 36 hpf. In (K), cfk−/− embryos have an increased end-diastolic diameter (on average 1.18× wild-type, p < 0.01) and do not generate blood flow at 36 hpf.(L and M) Increased bmp-4 expression at the AV boundary (red arrow) is observed in wild-type (L) and cfk−/− (M) embryos at 42 hpf in anticipation of endocardial ring formation.(N) Orientation of the embryos shown in (L) and (M). |
PMC406391_pbio-0020129-g001_101.jpg | What is the dominant medical problem in this image? | Embryos with Defective Myocardial Function Do Not Form AV ECs(A–C) Fluorescence micrographs of embryos carrying a tie2::GFP transgene, visualized at 48 hpf. In (A), the endocardial ring is visible as a collection of GFP-positive cells at the AV boundary in wild-type (wt) embryos (red arrow). In (B), sih−/− embryos fail to form an AV ring at 48 hpf. In (C), cfk−/− embryos fail to form an AV ring at 48 hpf.(D and E) Cushion development remains defective in cfk−/− embryos. In (D), a 5 μm hematoxylin and eosin-stained plastic section shows the initial stages of cushion development at the AV boundary (red arrows) in a 72 hpf wild-type embryo, with the ECs being two to three cell layers thick at this stage. In (E), a cfk
−/− embryo at 72 hpf shows dilation of both chambers of a blood-filled heart with no evidence of cushion formation at the AV boundary (red arrows).(F and G) cfk−/− embryos fail to form ECs at late stages. Embryos were visualized at identical magnification after counter-staining with rhodamine phalloidin. Red blood cells (RBCs) are seen in the atria of the hearts. In (F), confocal microscopy of a 96 hpf wild-type heart from a tie2::GFP line shows triangular ECs at the AV boundary (blue arrows). In (G), cfk−/− embryos at 96 hpf lack cushion formation and clustering of GFP-positive cells at the AV boundary (blue arrows).(H) At 72 hpf, wild-type embryos have narrow hearts with forward blood flow through the embryo.(I) At 72 hpf, cfk−/− embryos have dilated hearts filled with blood that regurgitates freely from the ventricle to the atrium.(J and K) The initial phenotype in cfk−/− embryos is cardiac dilation at 36 hpf. In (J), wild-type embryos have a narrow ventricle and generate pulsatile flow at 36 hpf. In (K), cfk−/− embryos have an increased end-diastolic diameter (on average 1.18× wild-type, p < 0.01) and do not generate blood flow at 36 hpf.(L and M) Increased bmp-4 expression at the AV boundary (red arrow) is observed in wild-type (L) and cfk−/− (M) embryos at 42 hpf in anticipation of endocardial ring formation.(N) Orientation of the embryos shown in (L) and (M). |
PMC406391_pbio-0020129-g001_110.jpg | Describe the main subject of this image. | Embryos with Defective Myocardial Function Do Not Form AV ECs(A–C) Fluorescence micrographs of embryos carrying a tie2::GFP transgene, visualized at 48 hpf. In (A), the endocardial ring is visible as a collection of GFP-positive cells at the AV boundary in wild-type (wt) embryos (red arrow). In (B), sih−/− embryos fail to form an AV ring at 48 hpf. In (C), cfk−/− embryos fail to form an AV ring at 48 hpf.(D and E) Cushion development remains defective in cfk−/− embryos. In (D), a 5 μm hematoxylin and eosin-stained plastic section shows the initial stages of cushion development at the AV boundary (red arrows) in a 72 hpf wild-type embryo, with the ECs being two to three cell layers thick at this stage. In (E), a cfk
−/− embryo at 72 hpf shows dilation of both chambers of a blood-filled heart with no evidence of cushion formation at the AV boundary (red arrows).(F and G) cfk−/− embryos fail to form ECs at late stages. Embryos were visualized at identical magnification after counter-staining with rhodamine phalloidin. Red blood cells (RBCs) are seen in the atria of the hearts. In (F), confocal microscopy of a 96 hpf wild-type heart from a tie2::GFP line shows triangular ECs at the AV boundary (blue arrows). In (G), cfk−/− embryos at 96 hpf lack cushion formation and clustering of GFP-positive cells at the AV boundary (blue arrows).(H) At 72 hpf, wild-type embryos have narrow hearts with forward blood flow through the embryo.(I) At 72 hpf, cfk−/− embryos have dilated hearts filled with blood that regurgitates freely from the ventricle to the atrium.(J and K) The initial phenotype in cfk−/− embryos is cardiac dilation at 36 hpf. In (J), wild-type embryos have a narrow ventricle and generate pulsatile flow at 36 hpf. In (K), cfk−/− embryos have an increased end-diastolic diameter (on average 1.18× wild-type, p < 0.01) and do not generate blood flow at 36 hpf.(L and M) Increased bmp-4 expression at the AV boundary (red arrow) is observed in wild-type (L) and cfk−/− (M) embryos at 42 hpf in anticipation of endocardial ring formation.(N) Orientation of the embryos shown in (L) and (M). |
PMC406391_pbio-0020129-g001_103.jpg | What's the most prominent thing you notice in this picture? | Embryos with Defective Myocardial Function Do Not Form AV ECs(A–C) Fluorescence micrographs of embryos carrying a tie2::GFP transgene, visualized at 48 hpf. In (A), the endocardial ring is visible as a collection of GFP-positive cells at the AV boundary in wild-type (wt) embryos (red arrow). In (B), sih−/− embryos fail to form an AV ring at 48 hpf. In (C), cfk−/− embryos fail to form an AV ring at 48 hpf.(D and E) Cushion development remains defective in cfk−/− embryos. In (D), a 5 μm hematoxylin and eosin-stained plastic section shows the initial stages of cushion development at the AV boundary (red arrows) in a 72 hpf wild-type embryo, with the ECs being two to three cell layers thick at this stage. In (E), a cfk
−/− embryo at 72 hpf shows dilation of both chambers of a blood-filled heart with no evidence of cushion formation at the AV boundary (red arrows).(F and G) cfk−/− embryos fail to form ECs at late stages. Embryos were visualized at identical magnification after counter-staining with rhodamine phalloidin. Red blood cells (RBCs) are seen in the atria of the hearts. In (F), confocal microscopy of a 96 hpf wild-type heart from a tie2::GFP line shows triangular ECs at the AV boundary (blue arrows). In (G), cfk−/− embryos at 96 hpf lack cushion formation and clustering of GFP-positive cells at the AV boundary (blue arrows).(H) At 72 hpf, wild-type embryos have narrow hearts with forward blood flow through the embryo.(I) At 72 hpf, cfk−/− embryos have dilated hearts filled with blood that regurgitates freely from the ventricle to the atrium.(J and K) The initial phenotype in cfk−/− embryos is cardiac dilation at 36 hpf. In (J), wild-type embryos have a narrow ventricle and generate pulsatile flow at 36 hpf. In (K), cfk−/− embryos have an increased end-diastolic diameter (on average 1.18× wild-type, p < 0.01) and do not generate blood flow at 36 hpf.(L and M) Increased bmp-4 expression at the AV boundary (red arrow) is observed in wild-type (L) and cfk−/− (M) embryos at 42 hpf in anticipation of endocardial ring formation.(N) Orientation of the embryos shown in (L) and (M). |
PMC406391_pbio-0020129-g001_104.jpg | What is the central feature of this picture? | Embryos with Defective Myocardial Function Do Not Form AV ECs(A–C) Fluorescence micrographs of embryos carrying a tie2::GFP transgene, visualized at 48 hpf. In (A), the endocardial ring is visible as a collection of GFP-positive cells at the AV boundary in wild-type (wt) embryos (red arrow). In (B), sih−/− embryos fail to form an AV ring at 48 hpf. In (C), cfk−/− embryos fail to form an AV ring at 48 hpf.(D and E) Cushion development remains defective in cfk−/− embryos. In (D), a 5 μm hematoxylin and eosin-stained plastic section shows the initial stages of cushion development at the AV boundary (red arrows) in a 72 hpf wild-type embryo, with the ECs being two to three cell layers thick at this stage. In (E), a cfk
−/− embryo at 72 hpf shows dilation of both chambers of a blood-filled heart with no evidence of cushion formation at the AV boundary (red arrows).(F and G) cfk−/− embryos fail to form ECs at late stages. Embryos were visualized at identical magnification after counter-staining with rhodamine phalloidin. Red blood cells (RBCs) are seen in the atria of the hearts. In (F), confocal microscopy of a 96 hpf wild-type heart from a tie2::GFP line shows triangular ECs at the AV boundary (blue arrows). In (G), cfk−/− embryos at 96 hpf lack cushion formation and clustering of GFP-positive cells at the AV boundary (blue arrows).(H) At 72 hpf, wild-type embryos have narrow hearts with forward blood flow through the embryo.(I) At 72 hpf, cfk−/− embryos have dilated hearts filled with blood that regurgitates freely from the ventricle to the atrium.(J and K) The initial phenotype in cfk−/− embryos is cardiac dilation at 36 hpf. In (J), wild-type embryos have a narrow ventricle and generate pulsatile flow at 36 hpf. In (K), cfk−/− embryos have an increased end-diastolic diameter (on average 1.18× wild-type, p < 0.01) and do not generate blood flow at 36 hpf.(L and M) Increased bmp-4 expression at the AV boundary (red arrow) is observed in wild-type (L) and cfk−/− (M) embryos at 42 hpf in anticipation of endocardial ring formation.(N) Orientation of the embryos shown in (L) and (M). |
PMC406391_pbio-0020129-g001_100.jpg | What key item or scene is captured in this photo? | Embryos with Defective Myocardial Function Do Not Form AV ECs(A–C) Fluorescence micrographs of embryos carrying a tie2::GFP transgene, visualized at 48 hpf. In (A), the endocardial ring is visible as a collection of GFP-positive cells at the AV boundary in wild-type (wt) embryos (red arrow). In (B), sih−/− embryos fail to form an AV ring at 48 hpf. In (C), cfk−/− embryos fail to form an AV ring at 48 hpf.(D and E) Cushion development remains defective in cfk−/− embryos. In (D), a 5 μm hematoxylin and eosin-stained plastic section shows the initial stages of cushion development at the AV boundary (red arrows) in a 72 hpf wild-type embryo, with the ECs being two to three cell layers thick at this stage. In (E), a cfk
−/− embryo at 72 hpf shows dilation of both chambers of a blood-filled heart with no evidence of cushion formation at the AV boundary (red arrows).(F and G) cfk−/− embryos fail to form ECs at late stages. Embryos were visualized at identical magnification after counter-staining with rhodamine phalloidin. Red blood cells (RBCs) are seen in the atria of the hearts. In (F), confocal microscopy of a 96 hpf wild-type heart from a tie2::GFP line shows triangular ECs at the AV boundary (blue arrows). In (G), cfk−/− embryos at 96 hpf lack cushion formation and clustering of GFP-positive cells at the AV boundary (blue arrows).(H) At 72 hpf, wild-type embryos have narrow hearts with forward blood flow through the embryo.(I) At 72 hpf, cfk−/− embryos have dilated hearts filled with blood that regurgitates freely from the ventricle to the atrium.(J and K) The initial phenotype in cfk−/− embryos is cardiac dilation at 36 hpf. In (J), wild-type embryos have a narrow ventricle and generate pulsatile flow at 36 hpf. In (K), cfk−/− embryos have an increased end-diastolic diameter (on average 1.18× wild-type, p < 0.01) and do not generate blood flow at 36 hpf.(L and M) Increased bmp-4 expression at the AV boundary (red arrow) is observed in wild-type (L) and cfk−/− (M) embryos at 42 hpf in anticipation of endocardial ring formation.(N) Orientation of the embryos shown in (L) and (M). |
PMC406391_pbio-0020129-g001_98.jpg | What key item or scene is captured in this photo? | Embryos with Defective Myocardial Function Do Not Form AV ECs(A–C) Fluorescence micrographs of embryos carrying a tie2::GFP transgene, visualized at 48 hpf. In (A), the endocardial ring is visible as a collection of GFP-positive cells at the AV boundary in wild-type (wt) embryos (red arrow). In (B), sih−/− embryos fail to form an AV ring at 48 hpf. In (C), cfk−/− embryos fail to form an AV ring at 48 hpf.(D and E) Cushion development remains defective in cfk−/− embryos. In (D), a 5 μm hematoxylin and eosin-stained plastic section shows the initial stages of cushion development at the AV boundary (red arrows) in a 72 hpf wild-type embryo, with the ECs being two to three cell layers thick at this stage. In (E), a cfk
−/− embryo at 72 hpf shows dilation of both chambers of a blood-filled heart with no evidence of cushion formation at the AV boundary (red arrows).(F and G) cfk−/− embryos fail to form ECs at late stages. Embryos were visualized at identical magnification after counter-staining with rhodamine phalloidin. Red blood cells (RBCs) are seen in the atria of the hearts. In (F), confocal microscopy of a 96 hpf wild-type heart from a tie2::GFP line shows triangular ECs at the AV boundary (blue arrows). In (G), cfk−/− embryos at 96 hpf lack cushion formation and clustering of GFP-positive cells at the AV boundary (blue arrows).(H) At 72 hpf, wild-type embryos have narrow hearts with forward blood flow through the embryo.(I) At 72 hpf, cfk−/− embryos have dilated hearts filled with blood that regurgitates freely from the ventricle to the atrium.(J and K) The initial phenotype in cfk−/− embryos is cardiac dilation at 36 hpf. In (J), wild-type embryos have a narrow ventricle and generate pulsatile flow at 36 hpf. In (K), cfk−/− embryos have an increased end-diastolic diameter (on average 1.18× wild-type, p < 0.01) and do not generate blood flow at 36 hpf.(L and M) Increased bmp-4 expression at the AV boundary (red arrow) is observed in wild-type (L) and cfk−/− (M) embryos at 42 hpf in anticipation of endocardial ring formation.(N) Orientation of the embryos shown in (L) and (M). |
PMC406391_pbio-0020129-g001_105.jpg | What is the dominant medical problem in this image? | Embryos with Defective Myocardial Function Do Not Form AV ECs(A–C) Fluorescence micrographs of embryos carrying a tie2::GFP transgene, visualized at 48 hpf. In (A), the endocardial ring is visible as a collection of GFP-positive cells at the AV boundary in wild-type (wt) embryos (red arrow). In (B), sih−/− embryos fail to form an AV ring at 48 hpf. In (C), cfk−/− embryos fail to form an AV ring at 48 hpf.(D and E) Cushion development remains defective in cfk−/− embryos. In (D), a 5 μm hematoxylin and eosin-stained plastic section shows the initial stages of cushion development at the AV boundary (red arrows) in a 72 hpf wild-type embryo, with the ECs being two to three cell layers thick at this stage. In (E), a cfk
−/− embryo at 72 hpf shows dilation of both chambers of a blood-filled heart with no evidence of cushion formation at the AV boundary (red arrows).(F and G) cfk−/− embryos fail to form ECs at late stages. Embryos were visualized at identical magnification after counter-staining with rhodamine phalloidin. Red blood cells (RBCs) are seen in the atria of the hearts. In (F), confocal microscopy of a 96 hpf wild-type heart from a tie2::GFP line shows triangular ECs at the AV boundary (blue arrows). In (G), cfk−/− embryos at 96 hpf lack cushion formation and clustering of GFP-positive cells at the AV boundary (blue arrows).(H) At 72 hpf, wild-type embryos have narrow hearts with forward blood flow through the embryo.(I) At 72 hpf, cfk−/− embryos have dilated hearts filled with blood that regurgitates freely from the ventricle to the atrium.(J and K) The initial phenotype in cfk−/− embryos is cardiac dilation at 36 hpf. In (J), wild-type embryos have a narrow ventricle and generate pulsatile flow at 36 hpf. In (K), cfk−/− embryos have an increased end-diastolic diameter (on average 1.18× wild-type, p < 0.01) and do not generate blood flow at 36 hpf.(L and M) Increased bmp-4 expression at the AV boundary (red arrow) is observed in wild-type (L) and cfk−/− (M) embryos at 42 hpf in anticipation of endocardial ring formation.(N) Orientation of the embryos shown in (L) and (M). |
PMC423138_pbio-0020163-g003_114.jpg | What key item or scene is captured in this photo? | Doxycycline and tTA-Dependent FCIP ExpressionImmunohistochemical assay (A–F) using rabbit polyclonal GFP antibodies/peroxidase-DAB system: (A) YC3.12, single-positive (MTH-YC3.12-7), double-positive (MTH-YC3.12-7, αCamKII-tTA), and Dox-treated double-positive (MTH-YC3.12-7, αCamKII-tTA).(B) Cg2, single-positive (MTH-Cg2-7) and doubles-positive (MTH-Cg2-7, αCamKII-tTA).(C) IP, single-positive (MTH-IP-12) and double-positive (MTH-IP-12, αCamKII-tTA).(D) Moderate-expression line of Cg2 (MTH-Cg2-14, αCamKII-tTA).(E) Low-expression line (MTH-Cg2-15, αCamKII-tTA).(F) FCIP distribution in various brain areas.(G) Fluorescence in fixed brain slices from the accessory and the main olfactory bulb.(H–K) Two-photon images of acute, living brain slices. (H) Neurons in both CA1 and striatum usually show nuclear exclusion. (I) punctate expression in low-expressing lines (also see Figure 2B, open circles); example from CA1 and cortex. Maximum intensity projection of two-photon 3D stacks taken from a brain slice (J) and a whole-mount retina (K). |
PMC423138_pbio-0020163-g003_116.jpg | Describe the main subject of this image. | Doxycycline and tTA-Dependent FCIP ExpressionImmunohistochemical assay (A–F) using rabbit polyclonal GFP antibodies/peroxidase-DAB system: (A) YC3.12, single-positive (MTH-YC3.12-7), double-positive (MTH-YC3.12-7, αCamKII-tTA), and Dox-treated double-positive (MTH-YC3.12-7, αCamKII-tTA).(B) Cg2, single-positive (MTH-Cg2-7) and doubles-positive (MTH-Cg2-7, αCamKII-tTA).(C) IP, single-positive (MTH-IP-12) and double-positive (MTH-IP-12, αCamKII-tTA).(D) Moderate-expression line of Cg2 (MTH-Cg2-14, αCamKII-tTA).(E) Low-expression line (MTH-Cg2-15, αCamKII-tTA).(F) FCIP distribution in various brain areas.(G) Fluorescence in fixed brain slices from the accessory and the main olfactory bulb.(H–K) Two-photon images of acute, living brain slices. (H) Neurons in both CA1 and striatum usually show nuclear exclusion. (I) punctate expression in low-expressing lines (also see Figure 2B, open circles); example from CA1 and cortex. Maximum intensity projection of two-photon 3D stacks taken from a brain slice (J) and a whole-mount retina (K). |
PMC423138_pbio-0020163-g003_117.jpg | What is being portrayed in this visual content? | Doxycycline and tTA-Dependent FCIP ExpressionImmunohistochemical assay (A–F) using rabbit polyclonal GFP antibodies/peroxidase-DAB system: (A) YC3.12, single-positive (MTH-YC3.12-7), double-positive (MTH-YC3.12-7, αCamKII-tTA), and Dox-treated double-positive (MTH-YC3.12-7, αCamKII-tTA).(B) Cg2, single-positive (MTH-Cg2-7) and doubles-positive (MTH-Cg2-7, αCamKII-tTA).(C) IP, single-positive (MTH-IP-12) and double-positive (MTH-IP-12, αCamKII-tTA).(D) Moderate-expression line of Cg2 (MTH-Cg2-14, αCamKII-tTA).(E) Low-expression line (MTH-Cg2-15, αCamKII-tTA).(F) FCIP distribution in various brain areas.(G) Fluorescence in fixed brain slices from the accessory and the main olfactory bulb.(H–K) Two-photon images of acute, living brain slices. (H) Neurons in both CA1 and striatum usually show nuclear exclusion. (I) punctate expression in low-expressing lines (also see Figure 2B, open circles); example from CA1 and cortex. Maximum intensity projection of two-photon 3D stacks taken from a brain slice (J) and a whole-mount retina (K). |
PMC423141_pbio-0020167-g002_122.jpg | What is the principal component of this image? | Mutant α-Actinin-4 Behavior in Cells(A) Mutant and wild-type α-actinin-4 show different localization and dynamics when expressed in a conditionally immortalized differentiated mouse podocyte cell line. Differentiated podocytes were injected in the nucleus with equal concentrations of expression plasmid for GFP fusions of mutant and wild-type actinins. At 2–4 h after injections, cells were imaged and both phase and fluorescence images recorded as described in the Materials and Methods. To illustrate changes in distribution of the fluorescence signal, three fluorescence images each 1 min apart were overlaid as red, green, and blue panes. Areas of fluorescence that were the same in all panes show as white, while dynamic areas are indicated by the color. The top panel indicates the initial phase and overlain dynamic fluorescence images of wild-type α-actinin-4, while the bottom two panels illustrate characteristic results for mutants K228E and T232I at 3 min time intervals. (See Videos S1–S3.)(B) Transfections in podocytes derived from mutant and wild-type mice. When transfected into conditionally immortalized podocytes of all three α-actinin-4 genotypes (+/+, K228E/+, or K228E/K228E), wild-type GFP–α-actinin-4 shows diffuse cytoskeletal localization. Mutant GFP–α-actinin-4 shows a similar alteration in localization when expressed in these three cells types. |
PMC423141_pbio-0020167-g002_121.jpg | What stands out most in this visual? | Mutant α-Actinin-4 Behavior in Cells(A) Mutant and wild-type α-actinin-4 show different localization and dynamics when expressed in a conditionally immortalized differentiated mouse podocyte cell line. Differentiated podocytes were injected in the nucleus with equal concentrations of expression plasmid for GFP fusions of mutant and wild-type actinins. At 2–4 h after injections, cells were imaged and both phase and fluorescence images recorded as described in the Materials and Methods. To illustrate changes in distribution of the fluorescence signal, three fluorescence images each 1 min apart were overlaid as red, green, and blue panes. Areas of fluorescence that were the same in all panes show as white, while dynamic areas are indicated by the color. The top panel indicates the initial phase and overlain dynamic fluorescence images of wild-type α-actinin-4, while the bottom two panels illustrate characteristic results for mutants K228E and T232I at 3 min time intervals. (See Videos S1–S3.)(B) Transfections in podocytes derived from mutant and wild-type mice. When transfected into conditionally immortalized podocytes of all three α-actinin-4 genotypes (+/+, K228E/+, or K228E/K228E), wild-type GFP–α-actinin-4 shows diffuse cytoskeletal localization. Mutant GFP–α-actinin-4 shows a similar alteration in localization when expressed in these three cells types. |
PMC423141_pbio-0020167-g002_124.jpg | What is shown in this image? | Mutant α-Actinin-4 Behavior in Cells(A) Mutant and wild-type α-actinin-4 show different localization and dynamics when expressed in a conditionally immortalized differentiated mouse podocyte cell line. Differentiated podocytes were injected in the nucleus with equal concentrations of expression plasmid for GFP fusions of mutant and wild-type actinins. At 2–4 h after injections, cells were imaged and both phase and fluorescence images recorded as described in the Materials and Methods. To illustrate changes in distribution of the fluorescence signal, three fluorescence images each 1 min apart were overlaid as red, green, and blue panes. Areas of fluorescence that were the same in all panes show as white, while dynamic areas are indicated by the color. The top panel indicates the initial phase and overlain dynamic fluorescence images of wild-type α-actinin-4, while the bottom two panels illustrate characteristic results for mutants K228E and T232I at 3 min time intervals. (See Videos S1–S3.)(B) Transfections in podocytes derived from mutant and wild-type mice. When transfected into conditionally immortalized podocytes of all three α-actinin-4 genotypes (+/+, K228E/+, or K228E/K228E), wild-type GFP–α-actinin-4 shows diffuse cytoskeletal localization. Mutant GFP–α-actinin-4 shows a similar alteration in localization when expressed in these three cells types. |
PMC423141_pbio-0020167-g002_128.jpg | What can you see in this picture? | Mutant α-Actinin-4 Behavior in Cells(A) Mutant and wild-type α-actinin-4 show different localization and dynamics when expressed in a conditionally immortalized differentiated mouse podocyte cell line. Differentiated podocytes were injected in the nucleus with equal concentrations of expression plasmid for GFP fusions of mutant and wild-type actinins. At 2–4 h after injections, cells were imaged and both phase and fluorescence images recorded as described in the Materials and Methods. To illustrate changes in distribution of the fluorescence signal, three fluorescence images each 1 min apart were overlaid as red, green, and blue panes. Areas of fluorescence that were the same in all panes show as white, while dynamic areas are indicated by the color. The top panel indicates the initial phase and overlain dynamic fluorescence images of wild-type α-actinin-4, while the bottom two panels illustrate characteristic results for mutants K228E and T232I at 3 min time intervals. (See Videos S1–S3.)(B) Transfections in podocytes derived from mutant and wild-type mice. When transfected into conditionally immortalized podocytes of all three α-actinin-4 genotypes (+/+, K228E/+, or K228E/K228E), wild-type GFP–α-actinin-4 shows diffuse cytoskeletal localization. Mutant GFP–α-actinin-4 shows a similar alteration in localization when expressed in these three cells types. |
PMC423141_pbio-0020167-g002_129.jpg | What is the core subject represented in this visual? | Mutant α-Actinin-4 Behavior in Cells(A) Mutant and wild-type α-actinin-4 show different localization and dynamics when expressed in a conditionally immortalized differentiated mouse podocyte cell line. Differentiated podocytes were injected in the nucleus with equal concentrations of expression plasmid for GFP fusions of mutant and wild-type actinins. At 2–4 h after injections, cells were imaged and both phase and fluorescence images recorded as described in the Materials and Methods. To illustrate changes in distribution of the fluorescence signal, three fluorescence images each 1 min apart were overlaid as red, green, and blue panes. Areas of fluorescence that were the same in all panes show as white, while dynamic areas are indicated by the color. The top panel indicates the initial phase and overlain dynamic fluorescence images of wild-type α-actinin-4, while the bottom two panels illustrate characteristic results for mutants K228E and T232I at 3 min time intervals. (See Videos S1–S3.)(B) Transfections in podocytes derived from mutant and wild-type mice. When transfected into conditionally immortalized podocytes of all three α-actinin-4 genotypes (+/+, K228E/+, or K228E/K228E), wild-type GFP–α-actinin-4 shows diffuse cytoskeletal localization. Mutant GFP–α-actinin-4 shows a similar alteration in localization when expressed in these three cells types. |
PMC449784_pbio-0020158-g003_138.jpg | What is the core subject represented in this visual? | GOF Planar Polarity Wing Phenotype of Fz1/2 Chimeras
dpp-Gal4 was used to express the respective Fz1/2 chimeras in the wing (same as described in Figure 2).(A) Wild-type wing. The dpp-Gal4 expression domain is highlighted by a thick orange line. In wild-type, all wing hairs are pointing distally.(B) dpp-Gal4; UAS-EGFP/UAS-fz1–1-1 wing (dpp>fz1–1-1; the expression domain is again highlighted with light orange). Wing hairs flanking the expression domain point away from it, consistent with previous observations that hair point away from higher levels of Fz1 activity (Adler et al. 1997).(C) dpp>fz1–2-2 wing. Wing hairs are not pointing away from expression domain, suggesting that Fz1–2-2 is not active for PCP signaling.(D) dpp>fz1–1-2 wing. Hairs point away only very slightly (less than 45 o; compare with Fz1–1-1, showing a 90 o reorientation next to expression domain). Several different lines of UAS-fz1–1-1 and UAS-fz1–1-2 were compared, showing identical behavior (Fz1–1-1 having a much stronger phenotype), suggesting that the C-tail is required for full PCP Fz activity.(E) dpp>fz2–1-1 wing. Most wing hairs point away from expression domain. The phenotype is weaker than Fz1–1-1.(F) dpp>fz1–2-1 wing. Wing hair orientation is hardly affected. Since Fz1–2-1 is apically localized (see Figure 2E), this result indicates that the presence of the Fz1 7-TM region is important for PCP activity. |
PMC449784_pbio-0020158-g003_136.jpg | What is the main focus of this visual representation? | GOF Planar Polarity Wing Phenotype of Fz1/2 Chimeras
dpp-Gal4 was used to express the respective Fz1/2 chimeras in the wing (same as described in Figure 2).(A) Wild-type wing. The dpp-Gal4 expression domain is highlighted by a thick orange line. In wild-type, all wing hairs are pointing distally.(B) dpp-Gal4; UAS-EGFP/UAS-fz1–1-1 wing (dpp>fz1–1-1; the expression domain is again highlighted with light orange). Wing hairs flanking the expression domain point away from it, consistent with previous observations that hair point away from higher levels of Fz1 activity (Adler et al. 1997).(C) dpp>fz1–2-2 wing. Wing hairs are not pointing away from expression domain, suggesting that Fz1–2-2 is not active for PCP signaling.(D) dpp>fz1–1-2 wing. Hairs point away only very slightly (less than 45 o; compare with Fz1–1-1, showing a 90 o reorientation next to expression domain). Several different lines of UAS-fz1–1-1 and UAS-fz1–1-2 were compared, showing identical behavior (Fz1–1-1 having a much stronger phenotype), suggesting that the C-tail is required for full PCP Fz activity.(E) dpp>fz2–1-1 wing. Most wing hairs point away from expression domain. The phenotype is weaker than Fz1–1-1.(F) dpp>fz1–2-1 wing. Wing hair orientation is hardly affected. Since Fz1–2-1 is apically localized (see Figure 2E), this result indicates that the presence of the Fz1 7-TM region is important for PCP activity. |
PMC449784_pbio-0020158-g003_139.jpg | What is the dominant medical problem in this image? | GOF Planar Polarity Wing Phenotype of Fz1/2 Chimeras
dpp-Gal4 was used to express the respective Fz1/2 chimeras in the wing (same as described in Figure 2).(A) Wild-type wing. The dpp-Gal4 expression domain is highlighted by a thick orange line. In wild-type, all wing hairs are pointing distally.(B) dpp-Gal4; UAS-EGFP/UAS-fz1–1-1 wing (dpp>fz1–1-1; the expression domain is again highlighted with light orange). Wing hairs flanking the expression domain point away from it, consistent with previous observations that hair point away from higher levels of Fz1 activity (Adler et al. 1997).(C) dpp>fz1–2-2 wing. Wing hairs are not pointing away from expression domain, suggesting that Fz1–2-2 is not active for PCP signaling.(D) dpp>fz1–1-2 wing. Hairs point away only very slightly (less than 45 o; compare with Fz1–1-1, showing a 90 o reorientation next to expression domain). Several different lines of UAS-fz1–1-1 and UAS-fz1–1-2 were compared, showing identical behavior (Fz1–1-1 having a much stronger phenotype), suggesting that the C-tail is required for full PCP Fz activity.(E) dpp>fz2–1-1 wing. Most wing hairs point away from expression domain. The phenotype is weaker than Fz1–1-1.(F) dpp>fz1–2-1 wing. Wing hair orientation is hardly affected. Since Fz1–2-1 is apically localized (see Figure 2E), this result indicates that the presence of the Fz1 7-TM region is important for PCP activity. |
PMC449784_pbio-0020158-g003_134.jpg | What object or scene is depicted here? | GOF Planar Polarity Wing Phenotype of Fz1/2 Chimeras
dpp-Gal4 was used to express the respective Fz1/2 chimeras in the wing (same as described in Figure 2).(A) Wild-type wing. The dpp-Gal4 expression domain is highlighted by a thick orange line. In wild-type, all wing hairs are pointing distally.(B) dpp-Gal4; UAS-EGFP/UAS-fz1–1-1 wing (dpp>fz1–1-1; the expression domain is again highlighted with light orange). Wing hairs flanking the expression domain point away from it, consistent with previous observations that hair point away from higher levels of Fz1 activity (Adler et al. 1997).(C) dpp>fz1–2-2 wing. Wing hairs are not pointing away from expression domain, suggesting that Fz1–2-2 is not active for PCP signaling.(D) dpp>fz1–1-2 wing. Hairs point away only very slightly (less than 45 o; compare with Fz1–1-1, showing a 90 o reorientation next to expression domain). Several different lines of UAS-fz1–1-1 and UAS-fz1–1-2 were compared, showing identical behavior (Fz1–1-1 having a much stronger phenotype), suggesting that the C-tail is required for full PCP Fz activity.(E) dpp>fz2–1-1 wing. Most wing hairs point away from expression domain. The phenotype is weaker than Fz1–1-1.(F) dpp>fz1–2-1 wing. Wing hair orientation is hardly affected. Since Fz1–2-1 is apically localized (see Figure 2E), this result indicates that the presence of the Fz1 7-TM region is important for PCP activity. |
PMC449784_pbio-0020158-g003_137.jpg | What is the focal point of this photograph? | GOF Planar Polarity Wing Phenotype of Fz1/2 Chimeras
dpp-Gal4 was used to express the respective Fz1/2 chimeras in the wing (same as described in Figure 2).(A) Wild-type wing. The dpp-Gal4 expression domain is highlighted by a thick orange line. In wild-type, all wing hairs are pointing distally.(B) dpp-Gal4; UAS-EGFP/UAS-fz1–1-1 wing (dpp>fz1–1-1; the expression domain is again highlighted with light orange). Wing hairs flanking the expression domain point away from it, consistent with previous observations that hair point away from higher levels of Fz1 activity (Adler et al. 1997).(C) dpp>fz1–2-2 wing. Wing hairs are not pointing away from expression domain, suggesting that Fz1–2-2 is not active for PCP signaling.(D) dpp>fz1–1-2 wing. Hairs point away only very slightly (less than 45 o; compare with Fz1–1-1, showing a 90 o reorientation next to expression domain). Several different lines of UAS-fz1–1-1 and UAS-fz1–1-2 were compared, showing identical behavior (Fz1–1-1 having a much stronger phenotype), suggesting that the C-tail is required for full PCP Fz activity.(E) dpp>fz2–1-1 wing. Most wing hairs point away from expression domain. The phenotype is weaker than Fz1–1-1.(F) dpp>fz1–2-1 wing. Wing hair orientation is hardly affected. Since Fz1–2-1 is apically localized (see Figure 2E), this result indicates that the presence of the Fz1 7-TM region is important for PCP activity. |
PMC449821_pbio-0020178-g009_140.jpg | Can you identify the primary element in this image? | Hairy Shows Context-Dependent Association with Its Cofactors(A) Sites of Hairy binding and Hairy cofactor recruitment based on DamID. The gray lines depict the relative position on the chromosomes of the approximately 6200 cDNAs on the microarray chip. The blue dots below the line represent Hairy binding sites while the green (Groucho), red (dCtBP), and yellow (dSir2) dots represent the positions of cofactor recruitment.(B–D) Cofactor recruitment visualized on third instar larval salivary gland chromosomes. Polytene chromosome sets stained (green) with antibodies to Groucho (B), dCtBP (C), and dSir2 (D). All chromosomes were counterstained with DAPI (blue) to visualize the DNA.(E) Higher magnification view of chromosome arms 2L and 2R costained with Groucho (red) and Hairy (green), and the merged image.(F) Higher magnification view of chromosome arm 2L costained with dCtBP (red) and Hairy (green), and the merged image, compared to the predicted DamID map. Note that both the DamID projected map and polytene chromosomes have more dCtBP recruitment sites to the left of the dashed line than to the right of the dashed line.(G) Chromosome arm 3R stained with dSir2 (green), highlighting regional specificity of dSir2 recruitment.(H and I) Higher magnification view of the distal ends of chromosome arms 2R (H) and 3L (I) from (D), stained with dSir2 (green), showing regional specificity and lack of dSir2 recruitment, respectively. |
PMC449821_pbio-0020178-g009_146.jpg | What is the principal component of this image? | Hairy Shows Context-Dependent Association with Its Cofactors(A) Sites of Hairy binding and Hairy cofactor recruitment based on DamID. The gray lines depict the relative position on the chromosomes of the approximately 6200 cDNAs on the microarray chip. The blue dots below the line represent Hairy binding sites while the green (Groucho), red (dCtBP), and yellow (dSir2) dots represent the positions of cofactor recruitment.(B–D) Cofactor recruitment visualized on third instar larval salivary gland chromosomes. Polytene chromosome sets stained (green) with antibodies to Groucho (B), dCtBP (C), and dSir2 (D). All chromosomes were counterstained with DAPI (blue) to visualize the DNA.(E) Higher magnification view of chromosome arms 2L and 2R costained with Groucho (red) and Hairy (green), and the merged image.(F) Higher magnification view of chromosome arm 2L costained with dCtBP (red) and Hairy (green), and the merged image, compared to the predicted DamID map. Note that both the DamID projected map and polytene chromosomes have more dCtBP recruitment sites to the left of the dashed line than to the right of the dashed line.(G) Chromosome arm 3R stained with dSir2 (green), highlighting regional specificity of dSir2 recruitment.(H and I) Higher magnification view of the distal ends of chromosome arms 2R (H) and 3L (I) from (D), stained with dSir2 (green), showing regional specificity and lack of dSir2 recruitment, respectively. |
PMC449821_pbio-0020178-g009_144.jpg | What is the focal point of this photograph? | Hairy Shows Context-Dependent Association with Its Cofactors(A) Sites of Hairy binding and Hairy cofactor recruitment based on DamID. The gray lines depict the relative position on the chromosomes of the approximately 6200 cDNAs on the microarray chip. The blue dots below the line represent Hairy binding sites while the green (Groucho), red (dCtBP), and yellow (dSir2) dots represent the positions of cofactor recruitment.(B–D) Cofactor recruitment visualized on third instar larval salivary gland chromosomes. Polytene chromosome sets stained (green) with antibodies to Groucho (B), dCtBP (C), and dSir2 (D). All chromosomes were counterstained with DAPI (blue) to visualize the DNA.(E) Higher magnification view of chromosome arms 2L and 2R costained with Groucho (red) and Hairy (green), and the merged image.(F) Higher magnification view of chromosome arm 2L costained with dCtBP (red) and Hairy (green), and the merged image, compared to the predicted DamID map. Note that both the DamID projected map and polytene chromosomes have more dCtBP recruitment sites to the left of the dashed line than to the right of the dashed line.(G) Chromosome arm 3R stained with dSir2 (green), highlighting regional specificity of dSir2 recruitment.(H and I) Higher magnification view of the distal ends of chromosome arms 2R (H) and 3L (I) from (D), stained with dSir2 (green), showing regional specificity and lack of dSir2 recruitment, respectively. |
PMC449870_pbio-0020207-g003_148.jpg | What is shown in this image? | FISH Confirmation of a Human-Specific Duplication of a Gene Cluster on Chromosome 5q13.3 Detected by Interspecies cDNA aCGH(A) Human duplication of a cluster of genes at Chromosome 5q13.3. is shown by two separate, and sometimes multiple, red BAC probe (CTD-2288G5) signals in interphase cells, with only one green BAC probe signal (RP11-1077O1) for a flanking region. Metaphase FISH shows both probes at band 5q13. The third nucleus in (A) shows four signals of the control probe (green) and eight copies of the BAC probe duplicated in the aCGH assay, consistent with the pattern expected in an S/G2 nucleus.(B–E) Bonobo (B), chimpanzee (C), gorilla (D), and orangutan (E) interphase FISH studies all show no increased signal for the human duplicated gene cluster, with signals of comparable size for the CTD-2288G5 (red) and the flanking RP11-107701 (green) probes. Metaphase FISH analyses show the gene cluster to be in the p arm of Chromosomes 4 (corresponding to the human Chromosome 5) in both the bonobo and chimpanzee, in the q arm of Chromosome 4 (corresponding to the human Chromosome 5) in the orangutan, and in the p arm of the gorilla Chromosome 19 (syntenic regions to human Chromosomes 5 and 17). |
PMC449870_pbio-0020207-g003_149.jpg | What's the most prominent thing you notice in this picture? | FISH Confirmation of a Human-Specific Duplication of a Gene Cluster on Chromosome 5q13.3 Detected by Interspecies cDNA aCGH(A) Human duplication of a cluster of genes at Chromosome 5q13.3. is shown by two separate, and sometimes multiple, red BAC probe (CTD-2288G5) signals in interphase cells, with only one green BAC probe signal (RP11-1077O1) for a flanking region. Metaphase FISH shows both probes at band 5q13. The third nucleus in (A) shows four signals of the control probe (green) and eight copies of the BAC probe duplicated in the aCGH assay, consistent with the pattern expected in an S/G2 nucleus.(B–E) Bonobo (B), chimpanzee (C), gorilla (D), and orangutan (E) interphase FISH studies all show no increased signal for the human duplicated gene cluster, with signals of comparable size for the CTD-2288G5 (red) and the flanking RP11-107701 (green) probes. Metaphase FISH analyses show the gene cluster to be in the p arm of Chromosomes 4 (corresponding to the human Chromosome 5) in both the bonobo and chimpanzee, in the q arm of Chromosome 4 (corresponding to the human Chromosome 5) in the orangutan, and in the p arm of the gorilla Chromosome 19 (syntenic regions to human Chromosomes 5 and 17). |
PMC449870_pbio-0020207-g003_150.jpg | What is the main focus of this visual representation? | FISH Confirmation of a Human-Specific Duplication of a Gene Cluster on Chromosome 5q13.3 Detected by Interspecies cDNA aCGH(A) Human duplication of a cluster of genes at Chromosome 5q13.3. is shown by two separate, and sometimes multiple, red BAC probe (CTD-2288G5) signals in interphase cells, with only one green BAC probe signal (RP11-1077O1) for a flanking region. Metaphase FISH shows both probes at band 5q13. The third nucleus in (A) shows four signals of the control probe (green) and eight copies of the BAC probe duplicated in the aCGH assay, consistent with the pattern expected in an S/G2 nucleus.(B–E) Bonobo (B), chimpanzee (C), gorilla (D), and orangutan (E) interphase FISH studies all show no increased signal for the human duplicated gene cluster, with signals of comparable size for the CTD-2288G5 (red) and the flanking RP11-107701 (green) probes. Metaphase FISH analyses show the gene cluster to be in the p arm of Chromosomes 4 (corresponding to the human Chromosome 5) in both the bonobo and chimpanzee, in the q arm of Chromosome 4 (corresponding to the human Chromosome 5) in the orangutan, and in the p arm of the gorilla Chromosome 19 (syntenic regions to human Chromosomes 5 and 17). |
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