PRC1 and PRC2 are not required for targeting of H2A.Z to developmental genes in embryonic stem cells

Robert S. Illingworth; Catherine H. Botting; Graeme R. Grimes; Wendy A. Bickmore; Ragnhild Eskeland

doi:10.1371/journal.pone.0034848

PRC1 and PRC2 are not required for targeting of H2A.Z to developmental genes in embryonic stem cells

Robert S. Illingworth, Catherine H. Botting, Graeme R. Grimes, Wendy A. Bickmore, Ragnhild Eskeland

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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.

Original language	English
Article number	e34848
Number of pages	13
Journal	PLoS ONE
Volume	7
Issue number	4
DOIs	https://doi.org/10.1371/journal.pone.0034848
Publication status	Published - 9 Apr 2012

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© 2012 Illingworth et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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title = "PRC1 and PRC2 are not required for targeting of H2A.Z to developmental genes in embryonic stem cells",

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.",

author = "Illingworth, {Robert S.} and Botting, {Catherine H.} and Grimes, {Graeme R.} and Bickmore, {Wendy A.} and Ragnhild Eskeland",

note = "This work was supported by the Medical Research Council, UK and by grant BB/H008500/1 from the BBSRC. ",

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AU - Illingworth, Robert S.

AU - Botting, Catherine H.

AU - Grimes, Graeme R.

AU - Bickmore, Wendy A.

AU - Eskeland, Ragnhild

N1 - This work was supported by the Medical Research Council, UK and by grant BB/H008500/1 from the BBSRC.

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N2 - 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.

AB - 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.

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PRC1 and PRC2 are not required for targeting of H2A.Z to developmental genes in embryonic stem cells

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