Biology Reference
In-Depth Information
(
Gao et al., 2012; Qin et al., 2012
), and SETDB1 represses some sets of devel-
opmental genes also targeted by the PcGpathway (
Bilodeau et al., 2009
). The
PRC1 subunits Cbx2 and Cbx7 have affinity for H3K27me3 and H3K9me3
in vitro
(
Bernstein et al., 2006; Kaustov et al., 2011
) andwere suggested to asso-
ciate with Suv39h KMT (
Li et al., 2010; Sewalt et al., 2002
). Suv39h KMT
could then influence PRC1 targeting as suggested by Yang and colleagues
(
Yang et al., 2011
), who showed that Cbx4/hPC2 localization in PcG is
dependent on Suv39h1 in quiescent cells. Interestingly, in the zygote,
PRC1 is prevented from binding to maternal PCH in a Suv39h2-dependent
manner (
Puschendorf et al., 2008
). Many of these enzymes and their relative
marks are present in germ cells of both sex and could therefore influence the
outcome of embryogenesis (
Brykczynska et al., 2010; Hammoud et al., 2009;
Posfai et al., 2012
). Though the concept of transgenerational inheritance is
still under debate (
Gill, Erkek, & Peters, 2012
), the interplay between these
two major chromatin silencing pathway would be an interesting way to
accommodate chromatin plasticity during developmental transition within
germ cell maturation and the developing embryo.
ACKNOWLEDGMENTS
M. T. greatly acknowledges his EMBO long-term fellowship and P. N. his Boehringer
Ingelheim Fonds PhD fellowship. Research in the Peters group is supported by the
Novartis Research Foundation, the Swiss National Science Foundation (NRP 63—Stem
Cells and Regenerative Medicine), SystemsX.ch (Cell plasticity), the Japanese Swiss
Science and Technology Cooperation Program, and the EMBO Young Investigator
Program.
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