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SUMMARY:A H3K9/H3K27 methylation crosstalk to repress gene expression in e
 mbryonic stem cells
DTSTART:20150108T103000
DTEND:20150108T113000
DTSTAMP:20260916T044025Z
UID:ed6da56771938c0f406bc9509f9c0d011fe8dc866b3c179c1e416eff
CATEGORIES:Conferences - Seminars
DESCRIPTION:Julien Pontis\, Ph.D. Université Paris Diderot Paris 7\, CNRS
  UMR 7216\, Paris (F)\nSEMINAR of the LAUSANNE INTEGRATIVE METABOLISM and 
 NUTRITION ALLIANCE (LIMNA)Abstract:\nG9a/GLP and Polycomb Repressive Compl
 ex 2 (PRC2) are two major epigenetic silencing machineries\, which in part
 icular methylate histone H3 on lysines 9 and 27 (H3K9 and H3K27)\, respect
 ively. Polycomb proteins are essential for maintaining gene repression dur
 ing development and consequently play pivotal roles in various biological 
 processes\, such as cellular pluripotency\, differentiation and plasticity
 . Although evidence of a crosstalk between H3K9 and H3K27 methylations has
  started to emerge\, their actual interplay remained elusive. Here\, we sh
 ow that PRC2 and G9a/GLP interact physically and functionally. Moreover\, 
 we show that G9a enzymatic activity modulates PRC2 genomic recruitment to 
 a subset of its target genes. Furthermore\, combining different genome-wid
 e approaches\, we demonstrate that PRC2 and G9a/GLP share an important num
 ber of common genomic targets\, encoding developmental and neuronal regula
 tors. Additionally\, we found genomic co-localization between G9a\, PRC2 a
 nd the neuronal regulator REST\, and showed that G9a forms a ternary compl
 ex with REST and PRC2. We could observe that one-third of G9a target sites
  co-localize with PRC2 and found G9a/PRC2 co-bound sites to be enriched ar
 ound promoters and CpG islands as compared to G9a alone. Interestingly\, t
 he G9a-binding sites\, excluding G9a/PRC2 co-bound sites\, are instead enr
 iched in LTRs. Taken together\, our findings reveal that the 'crosstalk' b
 etween H3K9 and H3K27 methylations is mediated\, at least in part\, by the
  G9a-mediated recruitment of PRC2 to a subset of genes. Interestingly\, we
  found that this mechanism is likely to be prevalent in the maintenance of
  neuronal gene silencing.
LOCATION:AI 1153 https://plan.epfl.ch/?room==AI%201153
STATUS:CONFIRMED
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