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H2BK5ac is an epigenetic modification to the DNA packaging protein Histone H2B. It is a mark that indicates the acetylation at the 5th lysine residue of the histone H2B protein. H2BK5ac is involved in maintaining stem cells and colon cancer

H2BK5ac

H3K4me1 is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the mono-methylation at the 4th lysine residue of the histone H3 protein and often associated with gene enhancers. Nomenclature H3K4me1 indicates monomethylation of lysine 4 on histone H3 protein subunit: Lysine methylation This diagram shows the progressive methylation of a lysine residue

H3K4me1

H3K4me3 is an epigenetic modification to the DNA packaging protein Histone H3 that indicates tri-methylation at the 4th lysine residue of the histone H3 protein and is often involved in the regulation of gene expression. The name denotes the addition of three methyl groups (trimethylation) to the lysine 4 on the histone H3 protein. H3 is used to package DNA in eukaryotic cells (including human cells), and modifications to the histone alter the accessibility of genes for transcription

H3K4me3

H3K9ac is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the acetylation at the 9th lysine residue of the histone H3 protein. The H3K9 histone has two jobs

H3K9ac

H3K9me2 is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the di-methylation at the 9th lysine residue of the histone H3 protein. H3K9me2 is strongly associated with transcriptional repression

H3K9me2

H3K9me3 is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the tri-methylation at the 9th lysine residue of the histone H3 protein and is often associated with heterochromatin. Nomenclature H3K9me3 indicates trimethylation of lysine 9 on histone H3 protein subunit: Lysine Methylation This diagram shows the progressive methylation of a lysine residue

H3K9me3

H3K14ac is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the acetylation at the 14th lysine residue of the histone H3 protein. H3K14ac has not been widely studied partly due to previous lack of commercially available antibody

H3K14ac

H3K23ac is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the acetylation at the 23rd lysine residue of the histone H3 protein. H3K23ac is not well studied but is correlated to TRIM24 in breast cancer

H3K23ac

H3K27ac is an epigenetic modification to the DNA packaging protein histone H3. It is a mark that indicates acetylation of the lysine residue at N-terminal position 27 of the histone H3 protein. H3K27ac is associated with the higher activation of transcription and therefore defined as an active enhancer mark

H3K27ac

H3K27me3 is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the tri-methylation of lysine 27 on histone H3 protein. This tri-methylation is associated with the downregulation of nearby genes via the formation of heterochromatic regions

H3K27me3

H3K36ac is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the acetylation at the 36th lysine residue of the histone H3 protein. H3K36ac has not been widely studied but it is very widely conserved across mammals and yeast and marks genes

H3K36ac

H3K36me is an epigenetic modification to the DNA packaging protein Histone H3, specifically, the mono-methylation at the 36th lysine residue of the histone H3 protein. There are diverse modifications at H3K36, such as phosphorylation, methylation, acetylation, and ubiquitylation, which have many important biological processes. The methylation of H3K36 has particularly had effects in transcriptional repression, alternative splicing, dosage compensation, DNA replication and repair, DNA methylation, and the transmission of the memory of gene expression from parents to offspring during development

H3K36me

H3K36me2 is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the di-methylation at the 36th lysine residue of the histone H3 protein. There are diverse modifications at H3K36 and have many important biological processes

H3K36me2

H3K36me3 is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the tri-methylation at the 36th lysine residue of the histone H3 protein and often associated with gene bodies. There are diverse modifications at H3K36 and have many important biological processes

H3K36me3

H3K56ac is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the acetylation at the 56th lysine residue of the histone H3 protein. It is a covalent modification known as a mark of newly replicated chromatin as well as replication-independent histone replacement

H3K56ac

H3K79me2 is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the di-methylation at the 79th lysine residue of the histone H3 protein. H3K79me2 is detected in the transcribed regions of active genes

H3K79me2

H3R2me2 is an epigenetic modification to the DNA packaging protein histone H3. It is a mark that indicates the di-methylation at the 2nd arginine residue of the histone H3 protein. In epigenetics, arginine methylation of histones H3 and H4 is associated with a more accessible chromatin structure and thus higher levels of transcription

H3R2me2

H3R8me2 is an epigenetic modification to the DNA packaging protein histone H3. It is a mark that indicates the di-methylation at the 8th arginine residue of the histone H3 protein. In epigenetics, arginine methylation of histones H3 and H4 is associated with a more accessible chromatin structure and thus higher levels of transcription

H3R8me2

H3R17me2 is an epigenetic modification to the DNA packaging protein histone H3. It is a mark that indicates the di-methylation at the 17th arginine residue of the histone H3 protein. In epigenetics, arginine methylation of histones H3 and H4 is associated with a more accessible chromatin structure and thus higher levels of transcription

H3R17me2

H3R26me2 is an epigenetic modification to the DNA packaging protein histone H3. It is a mark that indicates the di-methylation at the 26th arginine residue of the histone H3 protein. In epigenetics, arginine methylation of histones H3 and H4 is associated with a more accessible chromatin structure and thus higher levels of transcription

H3R26me2

H3R42me is an epigenetic modification to the DNA packaging protein histone H3. It is a mark that indicates the mono-methylation at the 42nd arginine residue of the histone H3 protein. In epigenetics, arginine methylation of histones H3 and H4 is associated with a more accessible chromatin structure and thus higher levels of transcription

H3R42me

H3S10P is an epigenetic modification to the DNA packaging protein histone H3. It is a mark that indicates the phosphorylation the 10th serine residue of the histone H3 protein. Depending on the environment in which it happens, the same phosphorylated residue might have drastically different consequences on chromatin structure

H3S10P

H3S28P is an epigenetic modification to the DNA packaging protein histone H3. It is a mark that indicates the phosphorylation the 28th serine residue of the histone H3 protein. Early mitosis phosphorylation patterns for H3S10 and H3S28 are quite similar, starting at the initiation of chromosomal condensation during prophase

H3S28P

H3T3P is an epigenetic modification to the DNA packaging protein histone H3. It is a mark that indicates the phosphorylation the 3rd threonine residue of the histone H3 protein. Pre-existing vs newly generated H3 is distinguished by phosphorylation at threonine 3

H3T3P

H3T6P is an epigenetic modification to the DNA packaging protein histone H3. It is a mark that indicates the phosphorylation of the 6th threonine residue of the histone H3 protein. H3S10P and H3T6P levels are higher in cervical cancer cells and are responsible for cellular transformation

H3T6P

H3T11P is an epigenetic modification to the DNA packaging protein histone H3. It is a mark that indicates the phosphorylation the 11th threonine residue of the histone H3 protein. Histone H3 phosphorylation at threonine 11 establishes a unique chromatin mark for transcriptional control

H3T11P

H3T45P is an epigenetic modification to the DNA packaging protein histone H3. It is a mark that indicates the phosphorylation the 45th threonine residue of the histone H3 protein. During apoptosis, H3T45 phosphorylation is required for structural changes inside the nucleosome that enable DNA nicking and/or fragmentation

H3T45P

H3Y41P is an epigenetic modification to the DNA packaging protein histone H3. It is a mark that indicates the phosphorylation the 41st tyrosine residue of the histone H3 protein. To impose cell cycle-dependent regulation of constitutive heterochromatin, H3Y41p collaborates with other regulatory mechanisms

H3Y41P

H4K5ac is an epigenetic modification to the DNA packaging protein histone H4. It is a mark that indicates the acetylation at the 5th lysine residue of the histone H4 protein. H4K5 is the closest lysine residue to the N-terminal tail of histone H4

H4K5ac

H4K8ac, representing an epigenetic modification to the DNA packaging protein histone H4, is a mark indicating the acetylation at the 8th lysine residue of the histone H4 protein. It has been implicated in the prevalence of malaria. Nomenclature H4K8ac indicates acetylation of lysine 8 on histone H4 protein subunit: Histone modifications The genomic DNA of eukaryotic cells is wrapped around special protein molecules known as histones

H4K8ac

H4K12ac is an epigenetic modification to the DNA packaging protein histone H4. It is a mark that indicates the acetylation at the 12th lysine residue of the histone H4 protein. H4K12ac is involved in learning and memory

H4K12ac

H4K16ac is an epigenetic modification to the DNA packaging protein Histone H4. It is a mark that indicates the acetylation at the 16th lysine residue of the histone H4 protein. H4K16ac is unusual in that it has both transcriptional activation AND repression activities

H4K16ac

H4K20me is an epigenetic modification to the DNA packaging protein Histone H4. It is a mark that indicates the mono-methylation at the 20th lysine residue of the histone H4 protein. This mark can be di- and tri-methylated

H4K20me

H4K91ac is an epigenetic modification to the DNA packaging protein histone H4. It is a mark that indicates the acetylation at the 91st lysine residue of the histone H4 protein. No known diseases are attributed to this mark but it might be implicated in melanoma

H4K91ac

H4R3me2 is an epigenetic modification to the DNA packaging protein histone H4. It is a mark that indicates the di-methylation at the 3rd arginine residue of the histone H4 protein. In epigenetics, arginine methylation of histones H3 and H4 is associated with a more accessible chromatin structure and thus higher levels of transcription

H4R3me2

Hard inheritance was a model of heredity that explicitly excludes any acquired characteristics, such as of Lamarckism. It is the exact opposite of soft inheritance, coined by Ernst Mayr to contrast ideas about inheritance. Hard inheritance states that characteristics of an organism's offspring (passed on through DNA) will not be affected by the actions that the parental organism performs during its lifetime

Hard inheritance

Edith Heard (born 1965) is a British-French researcher in epigenetics and since January 2019 has been the Director General of the European Molecular Biology Laboratory (EMBL). She is also Professor at the Collège de France, holding the Chair of Epigenetics and Cellular Memory. From 2010 to 2018, Heard was the Director of the Genetics and Developmental Biology department at the Curie Institute (Paris), France

Edith Heard

The family of heterochromatin protein 1 (HP1) ("Chromobox Homolog", CBX) consists of highly conserved proteins, which have important functions in the cell nucleus. These functions include gene repression by heterochromatin formation, transcriptional activation, regulation of binding of cohesion complexes to centromeres, sequestration of genes to the nuclear periphery, transcriptional arrest, maintenance of heterochromatin integrity, gene repression at the single nucleosome level, gene repression by heterochromatization of euchromatin, and DNA repair. HP1 proteins are fundamental units of heterochromatin packaging that are enriched at the centromeres and telomeres of nearly all eukaryotic chromosomes with the notable exception of budding yeast, in which a yeast-specific silencing complex of SIR (silent information regulatory) proteins serve a similar function

Heterochromatin protein 1

HIstome is a database that provides information about human histone proteins, their sites of modifications, variants and modifying enzymes, and diseases linked to histone modifications. Update HISTome2 is a updated version of the HIstome database released in 2020. See also Histone References External links http://www

HIstome

In biology, histones are highly basic proteins abundant in lysine and arginine residues that are found in eukaryotic cell nuclei. They act as spools around which DNA winds to create structural units called nucleosomes. Nucleosomes in turn are wrapped into 30-nanometer fibers that form tightly packed chromatin

Histone

Histone acetyltransferases (HATs) are enzymes that acetylate conserved lysine amino acids on histone proteins by transferring an acetyl group from acetyl-CoA to form ε-N-acetyllysine. DNA is wrapped around histones, and, by transferring an acetyl group to the histones, genes can be turned on and off. In general, histone acetylation increases gene expression

Histone acetyltransferase

The histone code is a hypothesis that the transcription of genetic information encoded in DNA is in part regulated by chemical modifications (known as histone marks) to histone proteins, primarily on their unstructured ends. Together with similar modifications such as DNA methylation it is part of the epigenetic code. Histones associate with DNA to form nucleosomes, which themselves bundle to form chromatin fibers, which in turn make up the more familiar chromosome

Histone code

Histone methylation is a process by which methyl groups are transferred to amino acids of histone proteins that make up nucleosomes, which the DNA double helix wraps around to form chromosomes. Methylation of histones can either increase or decrease transcription of genes, depending on which amino acids in the histones are methylated, and how many methyl groups are attached. Methylation events that weaken chemical attractions between histone tails and DNA increase transcription because they enable the DNA to uncoil from nucleosomes so that transcription factor proteins and RNA polymerase can access the DNA

Histone methylation

Histone methyltransferases (HMT) are histone-modifying enzymes (e. g. , histone-lysine N-methyltransferases and histone-arginine N-methyltransferases), that catalyze the transfer of one, two, or three methyl groups to lysine and arginine residues of histone proteins

Histone methyltransferase

(Histone-H3)-lysine-36 demethylase (EC 1. 14. 11

(Histone-H3)-lysine-36 demethylase

Histone-modifying enzymes are enzymes involved in the modification of histone substrates after protein translation and affect cellular processes including gene expression. To safely store the eukaryotic genome, DNA is wrapped around four core histone proteins (H3, H4, H2A, H2B), which then join to form nucleosomes. These nucleosomes further fold together into highly condensed chromatin, which renders the organism's genetic material far less accessible to the factors required for gene transcription, DNA replication, recombination and repair

Histone-modifying enzymes

HSV epigenetics is the epigenetic modification of herpes simplex virus (HSV) genetic code. As of 2012, an estimated 3. 7 billion people globally were infected with oral herpes simplex virus (HSV-1), and 417 million were living with genital herpes (HSV-2) worldwide (World Health Organization, 2018)

HSV epigenetics

Epigenetics of human development is the study of how epigenetics (hertiable characteristics that do no involve changes in DNA sequence) effects human development. Development before birth, including gametogenesis, embryogenesis, and fetal development, is the process of body development from the gametes are formed to eventually combine into a zygote to when the fully developed organism exits the uterus. Epigenetic processes are vital to fetal development due to the need to differentiate from a single cell to a variety of cell types that are arranged in such a way to produce cohesive tissues, organs, and systems

Epigenetics of human development

Human epigenome is the complete set of structural modifications of chromatin and chemical modifications of histones and nucleotides (such as cytosine methylation). These modifications affect according to cellular type and development status. Various studies show that epigenome depends on exogenous factors

Human epigenome

Induced stem cells (iSC) are stem cells derived from somatic, reproductive, pluripotent or other cell types by deliberate epigenetic reprogramming. They are classified as either totipotent (iTC), pluripotent (iPSC) or progenitor (multipotent – iMSC, also called an induced multipotent progenitor cell – iMPC) or unipotent – (iUSC) according to their developmental potential and degree of dedifferentiation. Progenitors are obtained by so-called direct reprogramming or directed differentiation and are also called induced somatic stem cells

Induced stem cells

The International Human Epigenome Consortium (IHEC) is a scientific organization, founded in 2010, that helps to coordinate global efforts in the field of Epigenomics. The initial goal was to generate at least 1,000 reference (baseline) human epigenomes from different types of normal and disease-related human cell types. Structure and funding IHEC's operations are funded by its full members (national and regional scientific funding agencies), and staffed largely on a volunteer basis by scientists and other experts from participating funding agencies and epigenome mapping projects

International Human Epigenome Consortium

A locus control region (LCR) is a long-range cis-regulatory element that enhances expression of linked genes at distal chromatin sites. It functions in a copy number-dependent manner and is tissue-specific, as seen in the selective expression of β-globin genes in erythroid cells. Expression levels of genes can be modified by the LCR and gene-proximal elements, such as promoters, enhancers, and silencers

Locus control region

Metabolic imprinting refers to the long-term physiological and metabolic effects that an offspring's prenatal and postnatal environments have on them. Perinatal nutrition has been identified as a significant factor in determining an offspring's likelihood of it being predisposed to developing cardiovascular disease, obesity, and type 2 diabetes amongst other conditions. During pregnancy, maternal glucose can cross the blood-placental barrier meaning maternal hyperglycaemia is associated with foetal hyperglycaemia

Metabolic imprinting

Methylated DNA immunoprecipitation (MeDIP or mDIP) is a large-scale (chromosome- or genome-wide) purification technique in molecular biology that is used to enrich for methylated DNA sequences. It consists of isolating methylated DNA fragments via an antibody raised against 5-methylcytosine (5mC). This technique was first described by Weber M

Methylated DNA immunoprecipitation

In the chemical sciences, methylation denotes the addition of a methyl group on a substrate, or the substitution of an atom (or group) by a methyl group. Methylation is a form of alkylation, with a methyl group replacing a hydrogen atom. These terms are commonly used in chemistry, biochemistry, soil science, and the biological sciences

Methylation

The missing heritability problem is the fact that single genetic variations cannot account for much of the heritability of diseases, behaviors, and other phenotypes. This is a problem that has significant implications for medicine, since a person's susceptibility to disease may depend more on the combined effect of all the genes in the background than on the disease genes in the foreground, or the role of genes may have been severely overestimated. The missing heritability problem was named as such in 2008 (after the "missing baryon problem" in physics)

Missing heritability problem

Histone-lysine N-methyltransferase 2A, also known as acute lymphoblastic leukemia 1 (ALL-1), myeloid/lymphoid or mixed-lineage leukemia 1 (MLL1), or zinc finger protein HRX (HRX), is an enzyme that in humans is encoded by the KMT2A gene. MLL1 is a histone methyltransferase deemed a positive global regulator of gene transcription. This protein belongs to the group of histone-modifying enzymes comprising transactivation domain 9aaTAD and is involved in the epigenetic maintenance of transcriptional memory

KMT2A

MORT (Mortal Obligate RNA Transcript (also known as ZNF667-AS1)) is a long non-coding RNA (lncRNA) of the intergenic type (lincRNA) that is specific to humans and great apes. The MORT transcript is produced in all mortal cell types, but is lost in a large fraction of the most common human cancers and therefore might have a tumor suppressive function. Genomic location The MORT gene is located on human chromosome 19, at position 56,989,000–57,007,000 (hg19) within a cluster of zinc finger genes (ZNF genes)

MORT (long non-coding RNA)

NAIL-MS (short for nucleic acid isotope labeling coupled mass spectrometry) is a technique based on mass spectrometry used for the investigation of nucleic acids and its modifications. It enables a variety of experiment designs to study the underlying mechanism of RNA biology in vivo. For example, the dynamic behaviour of nucleic acids in living cells, especially of RNA modifications, can be followed in more detail

NAIL-MS

The Epigenomics database at the National Center for Biotechnology Information was a database for whole-genome epigenetics data sets. It was retired on 1 June 2016. The Epigenomics database The Epigenomics database of the National Center for Biotechnology Information (NCBI) at the National Institutes of Health (NIH) was launched in June 2010 as a means to collect maps of epigenetic modifications and their occurrence across the human genome

NCBI Epigenomics

The neurobiological effects of physical exercise are numerous and involve a wide range of interrelated effects on brain structure, brain function, and cognition. A large body of research in humans has demonstrated that consistent aerobic exercise (e. g

Neurobiological effects of physical exercise

Neuroepigenetics is the study of how epigenetic changes to genes affect the nervous system. These changes may effect underlying conditions such as addiction, cognition, and neurological development. Mechanisms Neuroepigenetic mechanisms regulate gene expression in the neuron

Neuroepigenetics

In chromatin, those proteins which remain after the histones have been removed, are classified as non-histone proteins. The non-histone proteins, are a large group of heterogeneous proteins that play a role in organization and compaction of the chromosome into higher order structures. They play vital roles in regulating processes like nucleosome remodeling, DNA replication, RNA synthesis and processing, nuclear transport, steroid hormone action and interphase/mitosis transition

Non-histone protein

A nucleosome is the basic structural unit of DNA packaging in eukaryotes. The structure of a nucleosome consists of a segment of DNA wound around eight histone proteins and resembles thread wrapped around a spool. The nucleosome is the fundamental subunit of chromatin

Nucleosome

The nucleosome repeat length, (NRL) is the average distance between the centers of neighboring nucleosomes. NRL is an important physical chromatin property that determines its biological function. NRL can be determined genome-wide for the chromatin in a given cell type and state, or locally for a large enough genomic region containing several nucleosomes

Nucleosome repeat length

Nutriepigenomics is the study of food nutrients and their effects on human health through epigenetic modifications. There is now considerable evidence that nutritional imbalances during gestation and lactation are linked to non-communicable diseases, such as obesity, cardiovascular disease, diabetes, hypertension, and cancer. If metabolic disturbances occur during critical time windows of development, the resulting epigenetic alterations can lead to permanent changes in tissue and organ structure or function and predispose individuals to disease

Nutriepigenomics

Nutritional epigenetics is a science that studies the effects of nutrition on gene expression and chromatin accessibility. It is a subcategory of nutritional genomics that focuses on the effects of bioactive food components on epigenetic events. History Changes to children’s genetic profiles caused by fetal nutrition have been observed as early as the Dutch famine of 1944-1945

Nutritional epigenetics

In epigenetics, a paramutation is an interaction between two alleles at a single locus, whereby one allele induces a heritable change in the other allele. The change may be in the pattern of DNA methylation or histone modifications. The allele inducing the change is said to be paramutagenic, while the allele that has been epigenetically altered is termed paramutable

Paramutation

Pharmacoepigenetics is an emerging field that studies the underlying epigenetic marking patterns that lead to variation in an individual's response to medical treatment. Background Due to genetic heterogeneity, environmental factors, and pathophysiological causes, individuals that exhibit similar disease expression may respond differently to identical drug treatments. Selecting treatments based on factors such as age, body-surface area, weight, gender, or disease stage has been shown to incompletely address this problem, so medical professionals are shifting toward using patient genomic data to select optimal treatments

Pharmacoepigenetics

Position effect is the effect on the expression of a gene when its location in a chromosome is changed, often by translocation. This has been well described in Drosophila with respect to eye color and is known as position effect variegation (PEV). The phenotype is well characterised by unstable expression of a gene that results in the red eye coloration

Position effect

Probabilistic epigenesis is a way of understanding human behavior based on the relationship between experience and biology. It is a variant form of epigenetics, proposed by American psychologist Gilbert Gottlieb in 1991. Gottlieb’s model is based on Conrad H

Probabilistic epigenesis

In epigenetics, proline isomerization is the effect that cis-trans isomerization of the amino acid proline has on the regulation of gene expression. Similar to aspartic acid, the amino acid proline has the rare property of being able to occupy both cis and trans isomers of its prolyl peptide bonds with ease. Peptidyl-prolyl isomerase, or PPIase, is an enzyme very commonly associated with proline isomerization due to their ability to catalyze the isomerization of prolines

Proline isomerization in epigenetics

Protein methylation is a type of post-translational modification featuring the addition of methyl groups to proteins. It can occur on the nitrogen-containing side-chains of arginine and lysine, but also at the amino- and carboxy-termini of a number of different proteins. In biology, methyltransferases catalyze the methylation process, activated primarily by S-adenosylmethionine

Protein methylation

Generally, in progression to cancer, hundreds of genes are silenced or activated. Although silencing of some genes in cancers occurs by mutation, a large proportion of carcinogenic gene silencing is a result of altered DNA methylation (see DNA methylation in cancer). DNA methylation causing silencing in cancer typically occurs at multiple CpG sites in the CpG islands that are present in the promoters of protein coding genes

Regulation of transcription in cancer

In biology, reprogramming refers to erasure and remodeling of epigenetic marks, such as DNA methylation, during mammalian development or in cell culture. Such control is also often associated with alternative covalent modifications of histones. Reprogrammings that are both large scale (10% to 100% of epigenetic marks) and rapid (hours to a few days) occur at three life stages of mammals

Reprogramming

The epigenetics of schizophrenia is the study of how inherited epigenetic changes are regulated and modified by the environment and external factors and how these changes influence the onset and development of, and vulnerability to, schizophrenia. Epigenetics concerns the heritability of those changes, too. Schizophrenia is a debilitating and often misunderstood disorder that affects up to 1% of the world's population

Epigenetics of schizophrenia

A sex-determination system is a biological system that determines the development of sexual characteristics in an organism. Most organisms that create their offspring using sexual reproduction have two common sexes and a few less common intersex variations. In some species there are hermaphrodites

Sex-determination system

Sexual differentiation in humans is the process of development of sex differences in humans. It is defined as the development of phenotypic structures consequent to the action of hormones produced following gonadal determination. Sexual differentiation includes development of different genitalia and the internal genital tracts and body hair plays a role in sex identification

Sexual differentiation in humans

Single cell epigenomics is the study of epigenomics (the complete set of epigenetic modifications on the genetic material of a cell) in individual cells by single cell sequencing. Since 2013, methods have been created including whole-genome single-cell bisulfite sequencing to measure DNA methylation, whole-genome ChIP-sequencing to measure histone modifications, whole-genome ATAC-seq to measure chromatin accessibility and chromosome conformation capture. Single-cell DNA methylome sequencing Single cell DNA genome sequencing quantifies DNA methylation

Single cell epigenomics

Silent Information Regulator (SIR) proteins are involved in regulating gene expression. SIR proteins organize heterochromatin near telomeres, ribosomal DNA (rDNA), and at silent loci including hidden mating type loci in yeast. The SIR family of genes encodes catalytic and non-catalytic proteins that are involved in de-acetylation of histone tails and the subsequent condensation of chromatin around a SIR protein scaffold

SIR proteins

Skewed X-chromosome inactivation (skewed X-inactivation) occurs when the X-inactivation of one X chromosome is favored over the other, leading to an uneven number of cells with each chromosome inactivated. It is usually defined as one allele being found on the active X chromosome in over 75% of cells, and extreme skewing is when over 90% of cells have inactivated the same X chromosome. It can be caused by primary nonrandom inactivation, either by chance due to a small cell pool or directed by genes, or by secondary nonrandom inactivation, which occurs by selection

Skewed X-inactivation

Michael Kirtland Skinner is a U. S. biologist specializing in reproductive biology and epigenetics

Michael Skinner (biologist)

Sleep epigenetics is the field of how epigenetics (heritable characteristics that do not involve changes in DNA sequence) affects sleep. Research in the field of epigenetics has time and time again proven the significance of various environmental experiences. Changes in sleep can cause critical changes to the epigenome, while changes to the epigenome can, in turn, have a crucial influence on experiences related to sleep

Sleep epigenetics

Epigenetic effects of smoking concerns how epigenetics (hertiable characteristics that do not involve changes in DNA sequence) contributes to the deleterious effects of smoking. Cigarette smoking has been found to affect global epigenetic regulation of transcription across tissue types. Studies have shown differences in epigenetic markers like DNA methylation, histone modifications and miRNA expression between smokers and non-smokers

Epigenetic effects of smoking

A somatic epitype is a non-heritable epigenetic alteration in a gene. It is similar to conventional epigenetics in that it does not involve changes in the DNA primary sequence. Physically, the somatic epitype corresponds to changes in DNA methylation, oxidative damage (replacement of GTP with oxo-8-dGTP), or changes in DNA-chromatin structure that are not reversed by normal cellular or nuclear repair mechanisms

Somatic epitype

Structural inheritance or cortical inheritance is the transmission of an epigenetic trait in a living organism by a self-perpetuating spatial structures. This is in contrast to the transmission of digital information such as is found in DNA sequences, which accounts for the vast majority of known genetic variation. Examples of structural inheritance include the propagation of prions, the infectious proteins of diseases such as scrapie (in sheep and goats), bovine spongiform encephalopathy ('mad cow disease') and Creutzfeldt–Jakob disease (although the protein-only hypothesis of prion transmission has been considered contentious until recently)

Structural inheritance

Sex-determining region Y protein (SRY), or testis-determining factor (TDF), is a DNA-binding protein (also known as gene-regulatory protein/transcription factor) encoded by the SRY gene that is responsible for the initiation of male sex determination in therian mammals (placental mammals and marsupials). SRY is an intronless sex-determining gene on the Y chromosome. Mutations in this gene lead to a range of disorders of sex development with varying effects on an individual's phenotype and genotype

Sex-determining region Y protein

The TET enzymes are a family of ten-eleven translocation (TET) methylcytosine dioxygenases. They are instrumental in DNA demethylation. 5-Methylcytosine (see first Figure) is a methylated form of the DNA base cytosine (C) that often regulates gene transcription and has several other functions in the genome

TET enzymes

Transgenerational epigenetic inheritance is the transmission of epigenetic markers and modifications from one generation to multiple subsequent generations without altering the primary structure of DNA. Thus, the regulation of genes via epigenetic mechanisms can be heritable; the amount of transcripts and proteins produced can be altered by inherited epigenetic changes. In order for epigenetic marks to be heritable, however, they must occur in the gametes in animals, but since plants lack a definitive germline and can propagate, epigenetic marks in any tissue can be heritable

Transgenerational epigenetic inheritance

Transgenerational epigenetic inheritance in plants involves mechanisms for the passing of epigenetic marks from parent to offspring that differ from those reported in animals. There are several kinds of epigenetic markers, but they all provide a mechanism to facilitate greater phenotypic plasticity by influencing the expression of genes without altering the DNA code. These modifications represent responses to environmental input and are reversible changes to gene expression patterns that can be passed down through generations

Transgenerational epigenetic inheritance in plants

Epigenetics of anxiety and stress–related disorders is the field studying the relationship between epigenetic modifications of genes and anxiety and stress-related disorders, including mental health disorders such as generalized anxiety disorder (GAD), post-traumatic stress disorder, obsessive-compulsive disorder (OCD), and more. These change can lead to transgenerational stress inheritance. Epigenetic modifications play a role in the development and heritability of these disorders and related symptoms

Epigenetics of anxiety and stress–related disorders

Transvection is an epigenetic phenomenon that results from an interaction between an allele on one chromosome and the corresponding allele on the homologous chromosome. Transvection can lead to either gene activation or repression. It can also occur between nonallelic regions of the genome as well as regions of the genome that are not transcribed

Transvection (genetics)

X chromosome reactivation (XCR) is the process by which the inactive X chromosome (the Xi) is re-activated in the cells of eutherian female mammals. Therian female mammalian cells have two X chromosomes, while males have only one, requiring X-chromosome inactivation (XCI) for sex-chromosome dosage compensation. In eutherians, XCI is the random inactivation of one of the X chromosomes, silencing its expression

X-chromosome reactivation

X-inactivation (also called Lyonization, after English geneticist Mary Lyon) is a process by which one of the copies of the X chromosome is inactivated in therian female mammals. The inactive X chromosome is silenced by being packaged into a transcriptionally inactive structure called heterochromatin. As nearly all female mammals have two X chromosomes, X-inactivation prevents them from having twice as many X chromosome gene products as males, who only possess a single copy of the X chromosome (see dosage compensation)

X-inactivation

The Avery–MacLeod–McCarty experiment was an experimental demonstration, reported in 1944 by Oswald Avery, Colin MacLeod, and Maclyn McCarty, that DNA is the substance that causes bacterial transformation, in an era when it had been widely believed that it was proteins that served the function of carrying genetic information (with the very word protein itself coined to indicate a belief that its function was primary). It was the culmination of research in the 1930s and early 20th century at the Rockefeller Institute for Medical Research to purify and characterize the "transforming principle" responsible for the transformation phenomenon first described in Griffith's experiment of 1928: killed Streptococcus pneumoniae of the virulent strain type III-S, when injected along with living but non-virulent type II-R pneumococci, resulted in a deadly infection of type III-S pneumococci. In their paper "Studies on the Chemical Nature of the Substance Inducing Transformation of Pneumococcal Types: Induction of Transformation by a Desoxyribonucleic Acid Fraction Isolated from Pneumococcus Type III", published in the February 1944 issue of the Journal of Experimental Medicine, Avery and his colleagues suggest that DNA, rather than protein as widely believed at the time, may be the hereditary material of bacteria, and could be analogous to genes and/or viruses in higher organisms

Avery–MacLeod–McCarty experiment

C7 protein is an engineered zinc finger protein based on the murine ZFP, Zif268 and discovered by Wu et al. in 1994 (published in 1995). It shares the same zinc finger 2 and zinc finger 3 of Zif268, but differs in the sequence of finger 1

C7 protein

The C7. GAT protein is a zinc finger protein based on the C7 protein (itself based on the murine Zif268). It features an alternative zinc finger 3 alpha helix sequence, preventing the target site overlap caused by the aspartic acid residue of the finger 3 of C7

C7.GAT protein

Cell ablation (from Latin Cellula "small chamber" and Ablatio "removal"). Also known as tissue ablation, cell ablation is a biotechnological tool for studying cell lineage. The process consists of selectively destroying or removing cells in an organism

Cell ablation

Chimeric nucleases are an example of engineered proteins which must comprise a DNA-binding domain to give sequence specificity and a nuclease domain for DNA cleavage. DNA-binding domains DNA-binding domains including the basic helix-loop-helix, zinc finger, helix-turn-helix and leucine zipper motifs have been used in construction of sequence-specific nucleases. Of these, zinc fingers have been suggested the most important due to their modularity, allowing construction of a tailor-made DNA-binding domain

Chimeric nuclease

The Crick, Brenner et al. experiment (1961) was a scientific experiment performed by Francis Crick, Sydney Brenner, Leslie Barnett and R. J

Crick, Brenner et al. experiment