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'''Cellular memory modules''' are a form of [[Transgenerational epigenetic inheritance|epigenetic inheritance]] that allow cells to maintain their original identity after a series of [[Cell division|cell divisions]] and developmental processes. Cellular memory modules implement these preserved characteristics into transferred environments through [[transcriptional memory]].<ref>{{Citation |last=Paro |first=Renato |title=Cellular Memory |date=2021 |url=https://doi.org/10.1007/978-3-030-68670-3_3 |work=Introduction to Epigenetics |pages=49–66 |editor-last=Paro |editor-first=Renato |access-date=2023-04-20 |place=Cham |publisher=Springer International Publishing |language=en |doi=10.1007/978-3-030-68670-3_3 |isbn=978-3-030-68670-3 |last2=Grossniklaus |first2=Ueli |last3=Santoro |first3=Raffaella |last4=Wutz |first4=Anton |editor2-last=Grossniklaus |editor2-first=Ueli |editor3-last=Santoro |editor3-first=Raffaella |editor4-last=Wutz |editor4-first=Anton|doi-access=free |url-access=subscription }}</ref> Cellular memory modules are primarily found in ''[[Drosophila]]''.
== History ==
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== Locations and mechanisms: experiment overviews ==
[[File:Cell_memory_modules.jpg|thumb|PcG proteins repress transcription in salivary glands. A shows an active transcription. B shows transcription after addition of a promoter. C shows transcription of a mutant protein. D shows transcription become depressed.]]
Cellular memory modules have the same general process of genes undergoing [[Transcription (biology)|transcription]], these genes being transferred to an unfamiliar environment, and then these genes reverting to their original characteristics preserved through transcriptional memory. Cellular memory modules preserve repressed and active [[chromatin]] states in the [[Polycomb-group proteins|Polycomb group (PcG)]] and [[Trithorax-group proteins|trithorax group (trxG)]] proteins by using Polycomb- and trithorax [[response element]]s, which are just DNA sequences.<ref name="Déjardin-2004">{{Cite journal |last=Déjardin |first=Jérôme |last2=Cavalli |first2=Giacomo |date=2004-02-25 |title=Chromatin inheritance upon Zeste-mediated Brahma recruitment at a minimal cellular memory module |url=http://emboj.embopress.org/cgi/doi/10.1038/sj.emboj.7600108 |journal=The EMBO Journal |volume=23 |issue=4 |pages=857–868 |doi=10.1038/sj.emboj.7600108 |issn=0261-4189 |pmc=381013 |pmid=14963490}}</ref> Transcription resets and alters [[Epigenetic marker|epigenetic marks]] on chromosomal memory elements that are regulated by PcG and trxG proteins.<ref>{{Cite journal |last=Rank |first=Gerhard |last2=Prestel |first2=Matthias |last3=Paro |first3=Renato |date=2002-11-01 |title=Transcription through Intergenic Chromosomal Memory Elements of the Drosophila Bithorax Complex Correlates with an Epigenetic Switch |url=https://doi.org/10.1128/MCB.22.22.8026-8034.2002 |journal=Molecular and Cellular Biology |volume=22 |issue=22 |pages=8026–8034 |doi=10.1128/MCB.22.22.8026-8034.2002 |pmid=12391168|pmc=134728 }}</ref> PcG genes maintain silent expression states during the development of [[Hox gene|Hox genes]] while trxG proteins maintain Hox gene expression patterns. PcG proteins bind to Polycomb response elements (PREs) to repress the target gene and silence their transcription<ref>{{Cite journal |last=Bantignies |first=Frédéric |last2=Cavalli |first2=Giacomo |date=2006-06-01 |title=Cellular memory and dynamic regulation of polycomb group proteins |url=https://www.sciencedirect.com/science/article/pii/S0955067406000536 |journal=Current Opinion in Cell Biology |series=Nucleus and gene expression |language=en |volume=18 |issue=3 |pages=275–283 |doi=10.1016/j.ceb.2006.04.003 |issn=0955-0674|url-access=subscription }}</ref> by excluding [[transcriptional activators]] and making the gene unable to undergo RNA synthesis.<ref>{{Cite journal |last=Orlando |first=Valerio |date=2003-03-07 |title=Polycomb, Epigenomes, and Control of Cell Identity |url=https://www.cell.com/cell/abstract/S0092-8674(03)00157-0 |journal=Cell |language=English |volume=112 |issue=5 |pages=599–606 |doi=10.1016/S0092-8674(03)00157-0 |issn=0092-8674 |pmid=12628181|doi-access=free }}</ref> While the basis of the mechanism among cellular memory modules is the same, what initiates the mechanism and the specific proteins carrying it out differ based on the ___location of the cellular memory module within the gene. Some of these specific mechanisms and gene locations have been analyzed from experiments and outlined below.
=== Ab-Fab Mechanism ===
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=== Cancer Development ===
Misregulation of PcGs within cellular memory modules often leads to the development of [[Neoplasm|cancerous tumors]]. PcG’s role is to regulate the transcription of developmental genes, which entail processes like [[cell cycle]] progression, [[Cellular differentiation|differentiation]], or [[stem cell]] plasticity. Due to its imperative role in biological processes, mutations among PcGs initiate [[tumorigenesis]]. PcG mutations are more prominent among [[Hormone dependent cancers|hormone-dependent cancers]] where these proteins directly interact with the [[Hormone receptor|hormone receptors]]. It has been discovered that these PcG proteins are able to modulate the tumor microenvironment’s metabolism and immune response, impacting the cancer’s development. PcGs role in tumorigenesis isn’t fully understood although its link to cancer development is widely accepted.<ref>{{Cite journal |last=Parreno |first=Victoria |last2=Martinez |first2=Anne-Marie |last3=Cavalli |first3=Giacomo |date=March 2022 |title=Mechanisms of Polycomb group protein function in cancer |url=https://www.nature.com/articles/s41422-021-00606-6 |journal=Cell Research |language=en |volume=32 |issue=3 |pages=231–253 |doi=10.1038/s41422-021-00606-6 |issn=1748-7838|doi-access=free |pmc=8888700 }}</ref>
== References ==
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