Cfp1 is required for accurate H3K4me3 deposition in mouse ES cells

ABSTRACT: Trimethylation of histone H3 lysine 4 (H3K4me3) is a mark of active and poised promoters. The Set1 complex is responsible for most somatic H3K4me3 and contains the conserved subunit Cfp1, which binds to unmethylated CpGs and links H3K4me3 with CpG islands (CGIs). Here we report that Cfp1 plays unanticipated roles in organising genome wide H3K4me3 in embryonic stem cells. Cfp1-deficiency caused two contrasting phenotypes: drastic loss of H3K4me3 at expressed CGI-associated genes, with minimal consequences for transcription, and creation of ectopic H3K4me3 peaks at numerous regulatory regions. DNA binding by Cfp1 was dispensable for targeting H3K4me3 to active genes, but was required to prevent ectopic H3K4me3 peaks. We analysed gene expression in wild-type, Cfp1-/-, Cfp1wt rescue and Cfp1C1

ORGANISM(S): Mus musculus

SUBMITTER: THOMAS CLOUAIRE 

PROVIDER: E-MTAB-1198 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress