Normal Patterns of Histone H3K27 Methylation Require the Histone Variant H2A.Z in<i>Neurospora crassa</i>

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  • Abigail J Courtney
    Department of Microbiology, University of Georgia, Athens, Georgia 30602
  • Masayuki Kamei
    Department of Microbiology, University of Georgia, Athens, Georgia 30602
  • Aileen R Ferraro
    Department of Microbiology, University of Georgia, Athens, Georgia 30602
  • Kexin Gai
    State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University, Beijing 100193, China
  • Qun He
    State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University, Beijing 100193, China
  • Shinji Honda
    Division of Chromosome Biology, Faculty of Medical Sciences, University of Fukui, 910-1193, Japan
  • Zachary A Lewis
    Department of Microbiology, University of Georgia, Athens, Georgia 30602

説明

<jats:title>Abstract</jats:title><jats:p>Neurospora crassa contains a minimal Polycomb repression system, which provides rich opportunities to explore Polycomb-mediated repression across eukaryotes and enables genetic studies that can be difficult in plant and animal systems. Polycomb Repressive Complex 2 is a multi-subunit complex that deposits mono-, di-, and trimethyl groups on lysine 27 of histone H3, and trimethyl H3K27 is a molecular marker of transcriptionally repressed facultative heterochromatin. In mouse embryonic stem cells and multiple plant species, H2A.Z has been found to be colocalized with H3K27 methylation. H2A.Z is required for normal H3K27 methylation in these experimental systems, though the regulatory mechanisms are not well understood. We report here that Neurospora crassa mutants lacking H2A.Z or SWR-1, the ATP-dependent histone variant exchanger, exhibit a striking reduction in levels of H3K27 methylation. RNA-sequencing revealed downregulation of eed, encoding a subunit of PRC2, in an hH2Az mutant compared to wild type, and overexpression of EED in a ΔhH2Az;Δeed background restored most H3K27 methylation. Reduced eed expression leads to region-specific losses of H3K27 methylation, suggesting that differential dependence on EED concentration is critical for normal H3K27 methylation at certain regions in the genome.</jats:p>

収録刊行物

  • Genetics

    Genetics 216 (1), 51-66, 2020-09-01

    Oxford University Press (OUP)

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