Journal
NATURE COMMUNICATIONS
Volume 8, Issue -, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41467-017-00052-2
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Funding
- Wellcome Trust Strategic Award on Mouse Gastrulation
- Lister Institute
- Helmholtz Association
- EMBO [ASTF 336-2015]
- DGIST of the Ministry of Science, ICT and Future Planning [2017010073]
- Biotechnology and Biological Sciences Research Council [BBS/E/B/000C0404, BBS/E/B/000C0405] Funding Source: researchfish
- Cancer Research UK [22231] Funding Source: researchfish
- Medical Research Council [MR/L016311/1] Funding Source: researchfish
- BBSRC [BBS/E/B/000C0405, BBS/E/B/000C0404] Funding Source: UKRI
- MRC [MR/L016311/1] Funding Source: UKRI
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Polycomb repressive complexes (PRCs) are important histone modifiers, which silence gene expression; yet, there exists a subset of PRC-bound genes actively transcribed by RNA polymerase II (RNAPII). It is likely that the role of Polycomb repressive complex is to dampen expression of these PRC-active genes. However, it is unclear how this flipping between chromatin states alters the kinetics of transcription. Here, we integrate histone modifications and RNAPII states derived from bulk ChIP-seq data with single-cell RNA-sequencing data. We find that Polycomb repressive complex-active genes have greater cell-to-cell variation in expression than active genes, and these results are validated by knockout experiments. We also show that PRC-active genes are clustered on chromosomes in both two and three dimensions, and interactions with active enhancers promote a stabilization of gene expression noise. These findings provide new insights into how chromatin regulation modulates stochastic gene expression and transcriptional bursting, with implications for regulation of pluripotency and development.
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