Abstract
The essential histone variant H2A.Z localises to both active and silent chromatin sites. In embryonic stem cells (ESCs), H2A.Z is also reported to co-localise with polycomb repressive complex 2 (PRC2) at developmentally silenced genes. The mechanism of H2A.Z targeting is not clear, but a role for the PRC2 component Suz12 has been suggested. Given this association, we wished to determine if polycomb functionally directs H2A.Z incorporation in ESCs. We demonstrate that the PRC1 component Ring1B interacts with multiple complexes in ESCs. Moreover, we show that although the genomic distribution of H2A.Z co-localises with PRC2, Ring1B and with the presence of CpG islands, H2A.Z still blankets polycomb target loci in the absence of Suz12, Eed (PRC2) or Ring1B (PRC1). Therefore we conclude that H2A.Z accumulates at developmentally silenced genes in ESCs in a polycomb independent manner.
Highlights
Genome-wide mapping relative to cis-regulatory elements and transcriptionally active and repressed loci has implicated histone modifications in gene regulation
Proteomic analysis has identified that Ring1B is present in several complexes including PRC2 or Ring1B (PRC1), Bcl6 co-repressor complex (BcoR) and E2F6.com [21,22,23,24,25], a full analysis of Ring1B partners has not been examined in embryonic stem cells (ESCs)
We have previously shown that PRC1 components Phc2, Mel18 and Rybp are immunoprecipitated (IP’d) with Ring1B in mouse ESCs, while polycomb repressive complex 2 (PRC2) component Ezh2 did not interact [26]
Summary
Genome-wide mapping relative to cis-regulatory elements and transcriptionally active and repressed loci has implicated histone modifications in gene regulation. Another mechanism of chromatin regulation is the replacement of core histones with histone variants. Unlike the S-phase restricted expression of canonical histones, histone variants are expressed throughout the cell cycle. They have been implicated in the regulation of transcription, DNA repair, chromosome segregation and spermatogenesis [1]. In Drosophila embryos [3] and human CD4+ T cells [4], H2A.Z is enriched around the transcription start site (TSS) of active genes and it is incorporated into promoters of estrogen-receptor target genes upon their induction by estrogen [5]. In Saccharomyces cerevisiae H2A.Z is at promoters of both active and inactive genes [6] and prevents the spreading of telomeric heterochromatin into euchromatin [7,8]
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