Epigenetic memory: gene writer, eraser and homocysteine
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Epigenetic memory: gene writer, eraser and homocysteine Suresh C. Tyagi1 · Dragana Stanisic1,2 · Mahavir Singh1 Received: 12 May 2020 / Accepted: 31 August 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Naturally chromatin remodeling is highly organized, consisting of histone acetylation (opening/relaxation of the compact chromatin structure), DNA methylation (inhibition of the gene expression activity) and sequence rearrangement by shifting. All this is essentially required for proper “in-printing and off-printing” of genes thus ensuring the epigenetic memory process. Any imbalance in ratios of DNA methyltransferase (DNMT, gene writer), fat-mass obesity-associated protein (FTO, gene eraser) and product (function) homocysteine (Hcy) could lead to numerous diseases. Interestingly, a similar process also happens in stem cells during embryogenesis and development. Despite gigantic unsuccessful efforts undertaken thus far toward the conversion of a stem cell into a functional cardiomyocyte, there has been hardly any study that shows successful conversion of a stem cell into a multinucleated cardiomyocyte. We have shown nuclear hypertrophy during heart failure, however; the mechanism(s) of epigenetic memory, regulation of genes during fertilization, embryogenesis, development and during adulthood remain far from understanding. In addition, there may be a connection of aging, loosing of the memory leading to death, and presumably to reincarnation. This review highlights some of these pertinent issues facing the discipline of biology as a whole today. Keywords Chromatin remodeling · Nuclear MMP · 1-carbon (1-c) metabolism · Regenerative medicine · Stem cell · Heart failure · Growth retardation · Development · Embryogenesis Abbreviations DAAM Disheveled-associated activator of morphogenesis DNMT DNA methyltransferase FTO Fat-mass obesity-associated protein Hcy Homocysteine Met Methionine mTORC1 Mechanistic target of rapamycin complex 1 NLRP3 Nod-Like Receptor (NLR) Family Pyrin Domain Containing 3 PC Phosphatidylcholine PCP Phosphatidylcholine phosphatase * Mahavir Singh [email protected]; [email protected] 1
Department of Physiology, University of Louisville School of Medicine, Louisville, KY 40202, USA
Department of Dentistry, Faculty of Medical Sciences, University of Kragujevac, 34000 Kragujevac, Serbia
2
PE Phosphatidylethanolamine PEMT Phosphatidylethanolamine methyltransferase REDD1 Regulated in development DNA damage response 1 SAHH S-adenosine homocysteine hydrolase SAM S-adenosine methionine; SAH S-adenosine homocysteine TLR4, toll-like receptor-4
Background During embryogenesis and development the chromosome activation and inactivation is required for “imprinting and off-printing” of genes for the natural development (Fig. 1). The epigenetic DNA/RNA/protein methylation inhibits genes and in doing so generates homocysteine (Hcy), unequivocally. During development, genes are needed to be turned on and off. Histone acetylation relaxat
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