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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]]
▲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}}</ref>. Cellular memory modules are primarily found in ''[[Drosophila]]''.
== History ==
Cellular memory modules were discovered by [[François Jacob]] and [[Jacques Monod|Jaques Monod]] in 1961 at the [[Pasteur Institute]] in Paris. The discovery led to Jacob and Monod, along with [[André Michel Lwoff|André Lwoff]], receiving The Nobel Prize in Physiology or Medicine in 1965 for their discoveries regarding genetic control of enzyme and virus synthesis. These experimental results mapped the complex processes in which self-regulating processes express or suppress genes. Monod and Jacob proved how genetic information conversion during the [[Protein biosynthesis|construction of proteins]] was done through a messenger which evinced [[RNA]]
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[[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 [[
=== Ab-Fab Mechanism ===
This experiment was able to identify a minimal cellular memory module of 219 bp originating from the ''Drosophila Fab-7'' region which regulates the ''Abdominal-B'' gene. Recruitment of trxG proteins allows for binding to the [[DNA binding site|DNA binding sites]] on the Zeste protein, overriding Zeste’s need for the Brahma (BRM) protein, and initiating the inheritance of [[Active chromatin sequence|active chromatin]]. Researchers then took this Zeste protein and mutated its binding sites which increased its role in PcG-dependent silencing. Preserved DNA sequence Ab-''Fab'' recruits BRM and trxG proteins, activating [[Embryo|embryogenesis]] and weakening the bind of PcG to Zeste protein. The effects of Ab-''Fab'' allowed the Zeste protein to return to active chromatin states following its mutation. These response elements were determined to be cellular memory modules as there is DNA overlap and both elements express the memory of both silent and active chromatin by using cell division.<ref name="
=== H3K27 Mechanism ===
Polycomb repressive complexes (PRC) [[PRC1|1]] and 2 are recruited to bind to the [[H3K27me3]] gene, which is found at the beginning of ''Drosophila'' embryogenesis. [[PRC2]] then catalyzes the gene’s [[DNA methylation|methylation]], inducing PCR2 recruitment and compacting the chromatin. The research found that PRC2 recruitment is dependent on the presence of the H2AKub sequence. However, even after mutations in the H3K27 residue, PcGs were able to be recruited and revert to their original [[Phenotype|phenotypes]] indicating a transcriptional change in the H3K27 residue.<ref>{{Cite journal |last=Marasca |first=Federica |last2=Bodega |first2=Beatrice |last3=Orlando |first3=Valerio |date=April 2018
== Applications ==
=== Synthetic Memory Devices ===
Cellular memory modules are extremely beneficial to [[Synthetic biology|synthetic biologists]] as they are a form of transcriptional memory. Transcription is a well-understood biological process and completes a large amount of the cell’s information processing. Due to this, synthetic biologists can develop synthetic memory devices used in experiments that increase our understanding of cellular processes. These devices can record stimulus exposure, maintain [[gene expression]], and identify cell populations that respond to specific events along with tracking their progression throughout the response. This information can carry into disease research because if an event response correlates with future cell behavior, this can give scientists a greater understanding of diseases resulting from cellular inheritance like [[cancer]].<ref name="
=== 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
== References ==
{{reflist}}
[[Category:Cell biology]]
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