Introduction[edit]
Cellular memory modules are a form of epigenetic inheritance that allow cells to maintain their original identity after a series of cell divisions and developmental processes. Cellular memory modules implement these preserved characteristics into transferred environments through transcriptional memory [1]. Cellular memory modules are primarily found in Drosophila.
History
Cellular memory modules were discovered by François Jacob and Jaques Monod in 1961 at the Pasteur Institute in Paris. The discovery led to Jacob and Monod, along with 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 construction of proteins was done through a messenger which evinced RNA [2]. Lwoff aided in the experiment that won the Nobel Prize but did not work on the series of experiments that led to the discovery of cellular memory modules, which is why he remains uncredited in its discovery.
Cellular Memory Modules Locations and Mechanisms: Experiment Overviews
Cellular memory modules have the same general process of genes undergoing 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 (PcG) and trithorax group (trxG) proteins by using Polycomb- and trithorax response elements, which are just DNA sequences [3]. Transcription resets and alters epigenetic marks on chromosomal memory elements that are regulated by PcG and trxG proteins [4]. PcG genes maintain silent expression states during the development of 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[5] by excluding transcriptional activators and making the gene unable to undergo RNA synthesis[6]. 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.
References
- ^ Paro, Renato; Grossniklaus, Ueli; Santoro, Raffaella; Wutz, Anton (2021), Paro, Renato; Grossniklaus, Ueli; Santoro, Raffaella; Wutz, Anton (eds.), "Cellular Memory", Introduction to Epigenetics, Cham: Springer International Publishing, pp. 49–66, doi:10.1007/978-3-030-68670-3_3, ISBN 978-3-030-68670-3, retrieved 2023-04-20
- ^ "The Nobel Prize in Physiology or Medicine 1965". NobelPrize.org. Retrieved 2023-04-18.
- ^ Déjardin, Jérôme; Cavalli, Giacomo (2004-02-25). "Chromatin inheritance upon Zeste-mediated Brahma recruitment at a minimal cellular memory module". The EMBO Journal. 23 (4): 857–868. doi:10.1038/sj.emboj.7600108. ISSN 0261-4189. PMC 381013. PMID 14963490.
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: CS1 maint: PMC format (link) - ^ Rank, Gerhard; Prestel, Matthias; Paro, Renato (2002-11-01). "Transcription through Intergenic Chromosomal Memory Elements of the Drosophila Bithorax Complex Correlates with an Epigenetic Switch". Molecular and Cellular Biology. 22 (22): 8026–8034. doi:10.1128/MCB.22.22.8026-8034.2002. PMID 12391168.
- ^ Bantignies, Frédéric; Cavalli, Giacomo (2006-06-01). "Cellular memory and dynamic regulation of polycomb group proteins". Current Opinion in Cell Biology. Nucleus and gene expression. 18 (3): 275–283. doi:10.1016/j.ceb.2006.04.003. ISSN 0955-0674.
- ^ Orlando, Valerio (2003-03-07). "Polycomb, Epigenomes, and Control of Cell Identity". Cell. 112 (5): 599–606. doi:10.1016/S0092-8674(03)00157-0. ISSN 0092-8674. PMID 12628181.