User:Wikisabella/Epigenetics

Suggestions
Some aspects to this article are underdeveloped—covalent modifications (acetylation, ubiquitylation, phosphorylation, sumoylation, ribosylation, and citrullination), mRNA, sRNA, structural inheritance, early life stress, anxiety, and depression subsections, namely. There are a few sections which may have inappropriate sources/bias (early life stress—primary research source?).

Potential additions: mentioning UV radiation in DNA damage section, generally state mechanisms in DNA damage section, find more techniques/elucidate listed techniques, find information on histone state inheritability, explore acetylation, ubiquitylation, phosphorylation, sumoylation, ribosylation, and citrullination, find an update to RNA transcript section sperm research, expand both mRNA and sRNA discussions, find new data or explanations for structural inheritance, elucidate cancer, early life stress, addiction, anxiety, and depression sections.

Edits
[original] For example, acetylation of the K14 and K9 lysines of the tail of histone H3 by histone acetyltransferase enzymes (HATs) is generally related to transcriptional competence.[citation needed]

[edit] For example, acetylation of the K14 and K9 lysines of the tail of histone H3 by histone acetyltransferase enzymes (HATs) is known to regulate transcription in accordance with complementary histone deacetylases.

[new edition] Additionally, UV radiation is a common source of DNA damage, as both cyclobutane-pyrimidine dimers and 6-4 photoproducts (and their Dewar valance isomers) are created by UV radiation. Since cyclobutane-pyrimidine dimers and 6-4 photoproducts are the two most abundant mutagenic and cytotoxic DNA lesions, there are a host of DNA repair pathways enacted to confront these UV-induced lesions: excision repair, mutagenic repair, recombinational repair, cell-cycle checkpoints, and apoptosis.

[new addition] These repair pathways can be more generally referred to using broad categories for DNA repair, such as direct reversal mechanisms, excision repair mechanisms, and post-replication repair mechanisms.

[new addition] The chromatin landscape is recognized to be pivotal in composing the epigenome, and as such there are a variety of known mechanisms projected to allow for this chromatin landscape to be passed on. Among these mechanisms are models of histone recycling after replication, positive-feedback loops, long-range gene interactions, and networks of trans-acting factors.

[new subsection and text addition on aging] The aging phenotype—marked by functional decline of tissues and organs—is owed in large part to a changing epigenetic landscape. Specifically, changes in the methylation state of DNA has the consequence of perpetuating the aging phenotype, along with histone modifications, chromatin remodeling, and non-coding RNA misregulation. After research began revealing the substantial role epigenetics plays in creating the aging phenotype and promoting age-associated disease, a host of scientists globally have devoted themselves to finding potential interventions to the aging process that capitalize on these epigenetic markers. Furthermore, reduced methylation of DNA with age also functions simultaneously with higher variability in methylation sites—a finding that is particularly well visualized by looking at the epigenomes of monozygotic twins.