Cellular memory modules: Difference between revisions

Revision as of 15:12, 20 April 2023

Revision as of 15:13, 20 April 2023

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=== 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=":0" />.  

=== 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=2018-04 |title=How Polycomb-Mediated Cell Memory Deals With a Changing Environment: Variations in PcG complexes and proteins assortment convey plasticity to epigenetic regulation as a response to environment |url=https://onlinelibrary.wiley.com/doi/10.1002/bies.201700137 |journal=BioEssays |language=en |volume=40 |issue=4 |pages=1700137 |doi=10.1002/bies.201700137}}</ref>.

==References==