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Wiki Education Foundation-supported course assignment

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This article is or was the subject of a Wiki Education Foundation-supported course assignment. Further details are available on the course page. Student editor(s): Avouzas.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 19:03, 17 January 2022 (UTC)[reply]

Wiki Education Foundation-supported course assignment

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This article was the subject of a Wiki Education Foundation-supported course assignment, between 13 January 2020 and 6 May 2020. Further details are available on the course page. Student editor(s): Akhatan2016.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 19:03, 17 January 2022 (UTC)[reply]

Wiki Education Foundation-supported course assignment

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This article was the subject of a Wiki Education Foundation-supported course assignment, between 27 August 2019 and 6 December 2019. Further details are available on the course page. Student editor(s): Aae2019.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 17:39, 16 January 2022 (UTC)[reply]

Suggested edits to the aging section

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Hello everyone. I am a cellular and molecular biology graduate student assigned to editing a wiki page. I work with chromatin and aging and I would like to edit the aging section on this page to make it more comprehensive and up to date with the appropriate citations. In brief, I would like to modify the heading to senescence (different from, but still related to aging) and add text to describe global changes in chromatin structure, remodeler abundance, and epigenetic changes.

Suggested changes:

Senescence

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Chromatin architectural remodeling is implicated in the process of cellular senescence, which is related to, and yet distinct from, organismal aging. Replicative cellular senescence refers to a permanent cell cycle arrest where post-mitotic cells continue to exist as metabolically active cells but fail to proliferate[1][2]. Senescence can arise due to age associated degradation, telomere attrition, progerias, pre-malignancies, and other forms of damage or disease. Senescent cells undergo distinct repressive phenotypic changes, potentially to prevent the proliferation of damaged or cancerous cells, with modified chromatin organization, fluctuations in remodeler abundance, and changes in epigenetic modifications[3][4][1] .

Senescent cells undergo chromatin landscape modifications as constitutive heterochromatin migrates to the center of the nucleus and displaces euchromatin and facultative heterochromatin to regions at the edge of the nucleus. This disrupts chromatin-lamin interactions and inverts of the pattern typically seen in a mitotically active cell[5][3]. Individual Lamin-Associated Domains (LADs) and Topologically Associating Domains (TADs) are disrupted by this migration which can affect cis interactions across the genome[6]. Additionally, there is a general pattern of canonical histone loss, particularly in terms of the nucleosome histones H3 and H4 and the linker histone H1[5]. Histone variants with two exons are upregulated in senescent cells to produce modified nucleosome assembly which contributes to chromatin permissiveness to senescent changes.[6] Although transcription of variant histone proteins may be elevated, canonical histone proteins are not expressed as they are only made during the S phase of the cell cycle and senescent cells are post-mitotic.[5] During senescence, portions of chromosomes can be exported from the nucleus for lysosomal degradation which results in greater organizational disarray and disruption of chromatin interactions[4].

Chromatin remodeler abundance may be implicated in cellular senescence as knockdown or knockout of ATP-dependent remodelers such as NuRD, ACF1, and SWI/SNP can result in DNA damage and senescent phenotypes in yeast, C. elegans, mice, and human cell cultures[7][4][8] . ACF1 and NuRD are downregulated in senescent cells which suggests that chromatin remodeling is essential for maintaining a mitotic phenotype[7][8]. Genes involved in signaling for senescence can be silenced by chromatin confirmation and polycomb repressive complexes as seen in PRC1/PCR2 silencing of p16[9][10]. Specific remodeler depletion results in activation of proliferative genes through a failure to maintain silencing.[4] Some remodelers act on enhancer regions of genes rather than the specific loci to prevent re-entry into the cell cycle by forming regions of dense heterochromatin around regulatory regions[10].

Senescent cells undergo widespread fluctuations in epigenetic modifications in specific chromatin regions compared to mitotic cells. Human and murine cells undergoing replicative senescence experience a general global decrease in methylation; however, specific loci can differ from the general trend[11] [6] [4][9]. Specific chromatin regions, especially those around the promoters or enhancers of proliferative loci, may exhibit elevated methylation states with an overall imbalance of repressive and activating histone modifications[3]. Proliferative genes may show increases in the repressive mark H3K27me3 while genes involved in silencing or aberrant histone products may be enriched with the activating modification H3K4me3.[6] Additionally, upregulating histone deacetylases, such as members of the sirtuin family, can delay senescence by removing acetyl groups that contribute to greater chromatin accessibility[12]. General loss of methylation, combined with the addition of acetyl groups results in a more accessible chromatin conformation with a propensity towards disorganization when compared to mitotically active cells.[4] General loss of histones precludes addition of histone modifications and contributes changes in enrichment in some chromatin regions during senescence.[5]


References

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Aae2019 (talk) 19:39, 26 November 2019 (UTC)[reply]


lncRNA subsection under Cancer subsection. WIKI EDUCATION PROGRAM. FSU Graduate program Advanced Molecular Bio.

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I am a Grad student at FSU in the wiki education program for our Advanced Molecular Bio class. I am proposing to add a new subsection under the cancer subsection of the page, focusing on lncRNAs and different manners in which they can affect chromatin architecture and lead to the development and progression of different cancers. Additionally, I am proposing to add citations for the bullet points in the Cancer section and the bullet points in the Therapeutic intervention subsection.

Avouzas (talk) 18:22, 7 December 2017 (UTC)[reply]

LncRNAs

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The development of advanced sequencing technologies in the recent years has provided us with a more clear picture of what is being transcribed in the human genome. Despite only 2% of our DNA carrying protein-coding information, it is now clear that over 70% of the human genome is being transcribed. A large part of that 70% codes for long non-coding RNAs (lncRNAs), whose function we just started to explore in the last decade. However, it has been suggested that some are indirectly associated with different cancers through their association with chromatin-modification complexes, such as histone methyltransferases and the polycomb repressive complex 2 (PRC2)[13]. There is a number of lncRNAs that have been shown to associate with a number of different alterations in chromatin architecture in various cancers. These discoveries could provide with important insight as to the mechanisms of cancer development and metastasis as well as provide with diagnostic tools for certain forms of cancer.

One lncRNA associated with cancer is HOTAIR. Studies have shown that there is a correlation between HOTAIR and cancer metastasis. HOTAIR has been shown to regulate polycomp repressive complex 2 (PRC2) to affect chromatin organization and remodeling[14][4]. HOTAIR levels could also be used as a potential prognostic tool in certain types of cancer, including colorectal cancers among others[4]. Other ways lncRNAs could affect cancer development could be more indirect. For example, lncRNA HULC affects histone acetyl-transferase P300, by controlling levels of certain microRNAs and cAMP response element-binding protein (CREB), leading to alteration in deacetylation and methylation patterns in liver cancer[15]. Additionally, some lncRNAs can affect the density of chromatin. One such lncRNA is XIST RNA, which is correlated with heterochromatin defects in BRCA1-related breast cancers[16]. Finally, in some cases the absence of certain lncRNAs can be correlated with chromatin architecture alterations. In the case of certain colorectal cancers, a decrease in the expression of the LIT1/KCNQ1IT1 lncRNA is correlated with a decrease in H3K4 dimethylation and an enrichment in H3K9 dimethylation[17].

References

  1. ^ a b Parry, Aled John; Narita, Masashi (2016). "Old cells, new tricks: chromatin structure in senescence". Mammalian Genome. 27: 320–331. doi:10.1007/s00335-016-9628-9. ISSN 0938-8990. PMC 4935760. PMID 27021489.
  2. ^ Hayflick, L.; Moorhead, P. S. (1961-12-01). "The serial cultivation of human diploid cell strains". Experimental Cell Research. 25 (3): 585–621. doi:10.1016/0014-4827(61)90192-6. ISSN 0014-4827.
  3. ^ a b c Chandra, Tamir; Ewels, Philip Andrew; Schoenfelder, Stefan; Furlan-Magaril, Mayra; Wingett, Steven William; Kirschner, Kristina; Thuret, Jean-Yves; Andrews, Simon; Fraser, Peter; Reik, Wolf (2015-01-29). "Global Reorganization of the Nuclear Landscape in Senescent Cells". Cell Reports. 10 (4): 471–483. doi:10.1016/j.celrep.2014.12.055. ISSN 2211-1247. PMC 4542308. PMID 25640177.
  4. ^ a b c d e f g h Sun, Luyang; Yu, Ruofan; Dang, Weiwei (2018-04-16). "Chromatin Architectural Changes during Cellular Senescence and Aging". Genes. 9 (4). doi:10.3390/genes9040211. ISSN 2073-4425. PMC 5924553. PMID 29659513.{{cite journal}}: CS1 maint: unflagged free DOI (link) Cite error: The named reference ":3" was defined multiple times with different content (see the help page).
  5. ^ a b c d Criscione, Steven W.; Teo, Yee Voan; Neretti, Nicola (2016). "The chromatin landscape of cellular senescence". Trends in genetics : TIG. 32 (11): 751–761. doi:10.1016/j.tig.2016.09.005. ISSN 0168-9525. PMC 5235059. PMID 27692431.
  6. ^ a b c d Yang, Na; Sen, Payel (2018-11-03). "The senescent cell epigenome". Aging (Albany NY). 10 (11): 3590–3609. doi:10.18632/aging.101617. ISSN 1945-4589. PMC 6286853. PMID 30391936.
  7. ^ a b Basta, Jeannine; Rauchman, Michael (2015). "The Nucleosome Remodeling and Deacetylase (NuRD) Complex in Development and Disease". Translational research : the journal of laboratory and clinical medicine. 165 (1): 36–47. doi:10.1016/j.trsl.2014.05.003. ISSN 1931-5244. PMC 4793962. PMID 24880148.
  8. ^ a b Li, Xueping; Ding, Dong; Yao, Jun; Zhou, Bin; Shen, Ting; Qi, Yun; Ni, Ting; Wei, Gang (2019-07-15). "Chromatin remodeling factor BAZ1A regulates cellular senescence in both cancer and normal cells". Life Sciences. 229: 225–232. doi:10.1016/j.lfs.2019.05.023. ISSN 1879-0631. PMID 31085244.
  9. ^ a b López-Otín, Carlos; Blasco, Maria A.; Partridge, Linda; Serrano, Manuel; Kroemer, Guido (2013-06-06). "The Hallmarks of Aging". Cell. 153 (6): 1194–1217. doi:10.1016/j.cell.2013.05.039. ISSN 0092-8674. PMC 3836174. PMID 23746838.
  10. ^ a b Tasdemir, Nilgun; Banito, Ana; Roe, Jae-Seok; Alonso-Curbelo, Direna; Camiolo, Matthew; Tschaharganeh, Darjus F.; Huang, Chun-Hao; Aksoy, Ozlem; Bolden, Jessica E.; Chen, Chi-Chao; Fennell, Myles (2016). "BRD4 Connects Enhancer Remodeling to Senescence Immune Surveillance". Cancer Discovery. 6 (6): 612–629. doi:10.1158/2159-8290.CD-16-0217. ISSN 2159-8290. PMC 4893996. PMID 27099234.
  11. ^ Wilson, V. L.; Jones, P. A. (1983-06-03). "DNA methylation decreases in aging but not in immortal cells". Science (New York, N.Y.). 220 (4601): 1055–1057. doi:10.1126/science.6844925. ISSN 0036-8075. PMID 6844925.
  12. ^ Kaeberlein, Matt; McVey, Mitch; Guarente, Leonard (1999-10-01). "The SIR2/3/4 complex and SIR2 alone promote longevity in Saccharomyces cerevisiae by two different mechanisms". Genes & Development. 13 (19): 2570–2580. ISSN 0890-9369. PMID 10521401.
  13. ^ Fang, Yiwen; Fullwood, Melissa J. "Roles, Functions, and Mechanisms of Long Non-coding RNAs in Cancer". Genomics, Proteomics & Bioinformatics. 14 (1): 42–54. doi:10.1016/j.gpb.2015.09.006.
  14. ^ Gupta, Rajnish A.; Shah, Nilay; Wang, Kevin C.; Kim, Jeewon; Horlings, Hugo M.; Wong, David J.; Tsai, Miao-Chih; Hung, Tiffany; Argani, Pedram (2010/04). "Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis". Nature. 464 (7291): 1071–1076. doi:10.1038/nature08975. ISSN 1476-4687. {{cite journal}}: Check date values in: |date= (help)
  15. ^ Wang, Jiayi; Liu, Xiangfan; Wu, Huacheng; Ni, Peihua; Gu, Zhidong; Qiao, Yongxia; Chen, Ning; Sun, Fenyong; Fan, Qishi (2010-09-01). "CREB up-regulates long non-coding RNA, HULC expression through interaction with microRNA-372 in liver cancer". Nucleic Acids Research. 38 (16): 5366–5383. doi:10.1093/nar/gkq285. ISSN 0305-1048.
  16. ^ Sirchia, Silvia M.; Tabano, Silvia; Monti, Laura; Recalcati, Maria P.; Gariboldi, Manuela; Grati, Francesca R.; Porta, Giovanni; Finelli, Palma; Radice, Paolo (2009-05-15). "Misbehaviour of XIST RNA in Breast Cancer Cells". PLOS ONE. 4 (5): e5559. doi:10.1371/journal.pone.0005559. ISSN 1932-6203.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  17. ^ Nakano, Seiji; Murakami, Kazuhiro; Meguro, Makiko; Soejima, Hidenobu; Higashimoto, Ken; Urano, Takeshi; Kugoh, Hiroyuki; Mukai, Tsunehiro; Ikeguchi, Masahide (2006-11-01). "Expression profile of LIT1/KCNQ1OT1 and epigenetic status at the KvDMR1 in colorectal cancers". Cancer Science. 97 (11): 1147–1154. doi:10.1111/j.1349-7006.2006.00305.x. ISSN 1349-7006.
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