Biology:Chromatin variant

From HandWiki

A chromatin variant corresponds to a section of the genome that differs in chromatin states across cell types/states within an individual (intra-individual) or between individuals for a given cell type/state (inter-individual). Chromatin variants distinguish DNA sequences that differ in their function in one cell type/state versus another. Chromatin variants are found across the genome, inclusive of repetitive and non-repetitive DNA sequence.[1] Chromatin variants range in sizes. The smallest chromatin variants cover a few hundred DNA base pairs, such as seen at promoters, enhancers or insulators.[2][3][4][5][6] The largest chromatin variants capture a few thousand DNA base pairs, such as seen at Large Organized Chromatin Lysine domains (LOCKs)[7][8][9][10] and Clusters Of Cis-Regulatory Elements (COREs), such as super-enhancer.[11][12]

References

  1. ↑ Grillo, Giacomo; Lupien, Mathieu (June 2022). "Cancer-associated chromatin variants uncover the oncogenic role of transposable elements". Current Opinion in Genetics & Development 74: 101911. doi:10.1016/j.gde.2022.101911. ISSN 1879-0380. PMID 35487182. https://pubmed.ncbi.nlm.nih.gov/35487182. 
  2. ↑ "Discovery and characterization of chromatin states for systematic annotation of the human genome". Nature Biotechnology 28 (8): 817–25. August 2010. doi:10.1038/nbt.1662. PMID 20657582. 
  3. ↑ "FoxA1 translates epigenetic signatures into enhancer-driven lineage-specific transcription". Cell 132 (6): 958–70. March 2008. doi:10.1016/j.cell.2008.01.018. PMID 18358809. 
  4. ↑ "Distinct and predictive chromatin signatures of transcriptional promoters and enhancers in the human genome". Nature Genetics 39 (3): 311–8. March 2007. doi:10.1038/ng1966. PMID 17277777. 
  5. ↑ "Histone modifications at human enhancers reflect global cell-type-specific gene expression". Nature 459 (7243): 108–12. May 2009. doi:10.1038/nature07829. PMID 19295514. Bibcode: 2009Natur.459..108H. 
  6. ↑ Hoffman, Michael M.; Buske, Orion J.; Wang, Jie; Weng, Zhiping; Bilmes, Jeff A.; Noble, William Stafford (May 2012). "Unsupervised pattern discovery in human chromatin structure through genomic segmentation" (in en). Nature Methods 9 (5): 473–476. doi:10.1038/nmeth.1937. ISSN 1548-7105. PMID 22426492. 
  7. ↑ "Epigenetic Switch-Induced Viral Mimicry Evasion in Chemotherapy-Resistant Breast Cancer". Cancer Discovery 10 (9): 1312–1329. September 2020. doi:10.1158/2159-8290.CD-19-1493. PMID 32546577. 
  8. ↑ "Cancer as a dysregulated epigenome allowing cellular growth advantage at the expense of the host". Nature Reviews. Cancer 13 (7): 497–510. July 2013. doi:10.1038/nrc3486. PMID 23760024. 
  9. ↑ "Epigenomic reprogramming during pancreatic cancer progression links anabolic glucose metabolism to distant metastasis". Nature Genetics 49 (3): 367–376. March 2017. doi:10.1038/ng.3753. PMID 28092686. 
  10. ↑ "Large organized chromatin lysine domains help distinguish primitive from differentiated cell populations". Nature Communications 12 (1): 499. January 2021. doi:10.1038/s41467-020-20830-9. PMID 33479238. Bibcode: 2021NatCo..12..499M. 
  11. ↑ "Identifying clusters of cis-regulatory elements underpinning TAD structures and lineage-specific regulatory networks". Genome Research 29 (10): 1733–1743. October 2019. doi:10.1101/gr.248658.119. PMID 31533978. 
  12. ↑ "Super-enhancers in the control of cell identity and disease". Cell 155 (4): 934–47. November 2013. doi:10.1016/j.cell.2013.09.053. PMID 24119843. 



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