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Maternal histone variants and their chaperones promote paternal genome activation and boost somatic cell reprogramming
Author(s) -
Yang Peng,
Wu Warren,
Macfarlan Todd S.
Publication year - 2015
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/bies.201400072
Subject(s) - reprogramming , epigenome , somatic cell , biology , histone , epigenetics , histone methyltransferase , genetics , somatic cell nuclear transfer , dna methylation , zygote , histone code , histone methylation , microbiology and biotechnology , embryo , dna , cell , nucleosome , gene , embryogenesis , gene expression , blastocyst
The mammalian egg employs a wide spectrum of epigenome modification machinery to reprogram the sperm nucleus shortly after fertilization. This event is required for transcriptional activation of the paternal/zygotic genome and progression through cleavage divisions. Reprogramming of paternal nuclei requires replacement of sperm protamines with canonical and non‐canonical histones, covalent modification of histone tails, and chemical modification of DNA (notably oxidative demethylation of methylated cytosines). In this essay we highlight the role maternal histone variants play during developmental reprogramming following fertilization. We discuss how reduced maternal histone variant incorporation in somatic nuclear transfer experiments may explain the reduced viability of resulting embryos and how knowledge of repressive and activating maternal factors may be used to improve somatic cell reprogramming.