G9a-mediated irreversible epigenetic inactivation of Oct-3/4 during early embryogenesis

By Nirit Feldman, Ariela Gerson, Jia Fang, E. Li, Yi Zhang, Y. Shinkai, H. Cedar, Y. Bergman. Nature Cell Biology, 2006

691 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/e667f57ac2ceea05d4a3afaf5308aeb504c47cb3

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Citations in the corpus

Lineage-specific polycomb targets and de novo DNA methylation define restriction and potential of neuronal progenitors. (2008, background): “While such stabilization of an offstate has already been suggested for methylation at the Oct4 promoter (Feldman et al., 2006), we argue that this is likely to be a general mechanism for locking in the silent state of pluripotency- and germline-associated genes in order to prevent reactivation once ”
A combined chemical and genetic approach for the generation of induced pluripotent stem cells. (2008, positive): “This is consistent with the previous findings that the repressive H3K9 methylation is associated with Oct3/4 inactivation during differentiation (Feldman et al., 2006) and that histone lysine methylation is dynamic and regulated by HMTases and lysine demethylases.”
Chromatin challenges during DNA replication and repair. (2007, positive): “The importance of this deacetylation event for maturation of pericentromeric heterochromatin is illustrated by experiments in ﬁssion yeast and mouse cells where treatment with HDAC inhibitors interferes with HP1 binding and proper chromosome segregation (Ekwall et al., 1997; Taddei et al., 2001).”
How is pluripotency determined and maintained? (2007, background): “, 2005), these negative regulators might form the negative-feedback loop that shuts down Oct3/4 in differentiated cells, and which could then be followed by epigenetic chromatin modifications that result in the repression of the Oct3/4 promoter (Feldman et al., 2006).”
Induced pluripotency: history, mechanisms, and applications. (2010, background): “This effect is consistent with G9a’s role in the post-implantation embryo, where it is involved in the stable epigenetic silencing of Oct4 (Feldman et al. 2006).”
Epigenetic reprogramming and induced pluripotency (2009, background): “Prior to de novo DNA methylation, Oct4 can be readily reactivated when differentiating cells are returned to ES cell culture conditions (Feldman et al., 2006), indicating that only DNA methylation stably locks in the repressed state.”
Polycomb-mediated methylation on Lys27 of histone H3 pre-marks genes for de novo methylation in cancer (2007, background): “All of these post-implantation events seem to be accompanied by heterochromatization, involving the local methylation of histone H3 on either lysine 9 (H3K9; ref”
Stability and flexibility of epigenetic gene regulation in mammalian development (2007, background): “Several genes that are required for early development or for germ-cell development only — for example, those that encode pluripotency-sustaining transcription factors (such as OCT4 and NANOG) — are known to be expressed by ES cells but silenced on the differentiation of these cells, with a defined k”
Control of Embryonic Stem Cell State (2011, background): “Silencing of the Pou5f1 gene is mediated by trans-acting repressors such as ARP-1, COUP-TF1, and GCNF, nucleosome modification by the G9a H3K9 methyltransferase, and promoter DNA methylation by Dnmt3a/3b (Ben-Shushan et al., 1995; Feldman et al., 2006; Fuhrmann et al., 2001).”
DGCR8 is essential for microRNA biogenesis and silencing of embryonic stem cell self-renewal (2007, background): “In addition, the G9a histone methyltransferase and the Dnmt3a and Dnmt3b DNA methyltransferases have been reported to be essential for maintaining differentiation of ES cells after retinoic acid treatmen”
Induction of pluripotent stem cells from mouse embryonic fibroblasts by Oct4 and Klf4 with small-molecule compounds. (2008, background): “Ce G9a target genes (Feldman et al., 2006).”
Linking DNA methylation and histone modification: patterns and paradigms (2009, background): “In the final stage of silencing, the G9a-containing complex also recruits DNMT3A and DNMT3B, which catalyse de novo DNA methylation at the promote”