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.[1]

[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.[2]

[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.[3]

[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.[4]

[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.[5] 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.[6]

Bibliography

UV-induced DNA damage, repair mechanisms, methods of detecting damage.[2]

Mechanisms for repairing different types of DNA damage.[3]

BioRad methods for studying epigenetics.[7]

Information on the inheritance of chromatin structure/histone state inheritability.[8]

Non-coding RNAs, miRNAs, siRNAs, piRNAs, and lncRNAs relationship to epigenetics.[9]

Chromatin structural influence on epigenetic inheritance.[4]

Example of application for epigenetics to improve cancer treatment/detection.[10]

Trans-generational inheritance of epigenetic changes.[11]

Nazi occupation and trans-generational inheritance post-malnutrition.[12]

  1. ^ Berndsen, Christopher E.; Denu, John M. (2009). "Catalysis and Substrate Selection by Histone/Protein Lysine Acetyltransferases". Current opinion in structural biology. 18 (6): 682–689. doi:10.1016/j.sbi.2008.11.004. ISSN 0959-440X. PMC 2723715. PMID 19056256.
  2. ^ a b Sinha, Rajeshwar P.; Häder, Donat P. (2002–2004). "UV-induced DNA damage and repair: a review". Photochemical & Photobiological Sciences: Official Journal of the European Photochemistry Association and the European Society for Photobiology. 1 (4): 225–236. doi:10.1039/b201230h. ISSN 1474-905X. PMID 12661961.{{cite journal}}: CS1 maint: date format (link)
  3. ^ a b Cooper, Geoffrey M. (2000). "DNA Repair". The Cell: A Molecular Approach. 2nd edition.
  4. ^ a b Margueron, Raphaël; Reinberg, Danny (2010). "Chromatin structure and the inheritance of epigenetic information". Nature Reviews Genetics. 11 (4): 285–296. doi:10.1038/nrg2752. ISSN 1471-0064.
  5. ^ Cakouros, Dimitrios; Gronthos, Stan (2019). "Epigenetic Regulation of Bone Marrow Stem Cell Aging: Revealing Epigenetic Signatures associated with Hematopoietic and Mesenchymal Stem Cell Aging". Aging and disease. 10 (1): 174. doi:10.14336/ad.2017.1213. ISSN 2152-5250.
  6. ^ Jones, Meaghan J.; Goodman, Sarah J.; Kobor, Michael S. (2015-12). "DNA methylation and healthy human aging". Aging Cell. 14 (6): 924–932. doi:10.1111/acel.12349. ISSN 1474-9718. PMC 4693469. PMID 25913071. {{cite journal}}: Check date values in: |date= (help)CS1 maint: unflagged free DOI (link)
  7. ^ "Epigenetics Analysis | LSR | Bio-Rad". www.bio-rad.com. Retrieved 2020-03-06.
  8. ^ Smith, Christine M.; Haimberger, Zara W.; Johnson, Catherine O.; Wolf, Alex J.; Gafken, Philip R.; Zhang, Zhongli; Parthun, Mark R.; Gottschling, Daniel E. (2002-12-10). "Heritable chromatin structure: Mapping "memory" in histones H3 and H4". Proceedings of the National Academy of Sciences of the United States of America. 99 (Suppl 4): 16454–16461. doi:10.1073/pnas.182424999. ISSN 0027-8424. PMID 12196632.
  9. ^ Wei, Jian-Wei; Huang, Kai; Yang, Chao; Kang, Chun-Sheng (2017-01-01). "Non-coding RNAs as regulators in epigenetics (Review)". Oncology Reports. 37 (1): 3–9. doi:10.3892/or.2016.5236. ISSN 1021-335X.
  10. ^ Wong, Ee Ming; Southey, Melissa C.; Terry, Mary Beth (2020-02-18). "Integrating DNA methylation measures to improve clinical risk assessment: are we there yet? The case of BRCA1 methylation marks to improve clinical risk assessment of breast cancer". British Journal of Cancer: 1–8. doi:10.1038/s41416-019-0720-2. ISSN 1532-1827.
  11. ^ Horsthemke, Bernhard (2018-07-30). "A critical view on transgenerational epigenetic inheritance in humans". Nature Communications. 9 (1): 1–4. doi:10.1038/s41467-018-05445-5. ISSN 2041-1723.
  12. ^ Pembrey, Marcus; Saffery, Richard; Bygren, Lars Olov (2014-9). "Human transgenerational responses to early-life experience: potential impact on development, health and biomedical research". Journal of Medical Genetics. 51 (9): 563–572. doi:10.1136/jmedgenet-2014-102577. ISSN 0022-2593. PMC 4157403. PMID 25062846. {{cite journal}}: Check date values in: |date= (help)

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