Direct interrogation of the role of H3K9 in metazoan heterochromatin function Public Deposited

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  • Matera, Gregory
    • Affiliation: School of Medicine, Department of Genetics, College of Arts and Sciences, Department of Biology, Integrative Program for Biological and Genome Sciences, N.C. Cancer Hospital, UNC Lineberger Comprehensive Cancer Center, Curriculum in Genetics and Molecular Biology
  • Strahl, Brian
    • Affiliation: N.C. Cancer Hospital, UNC Lineberger Comprehensive Cancer Center, School of Medicine, Department of Biochemistry and Biophysics, Curriculum in Genetics and Molecular Biology
  • Penke, Taylor J.R.
    • Affiliation: School of Medicine, Curriculum in Genetics and Molecular Biology
  • McKay, Daniel
    • Affiliation: School of Medicine, Department of Genetics, College of Arts and Sciences, Department of Biology, Integrative Program for Biological and Genome Sciences, Curriculum in Genetics and Molecular Biology
  • Duronio, Robert
    • Affiliation: School of Medicine, Department of Genetics, College of Arts and Sciences, Department of Biology, Integrative Program for Biological and Genome Sciences, N.C. Cancer Hospital, UNC Lineberger Comprehensive Cancer Center, Curriculum in Genetics and Molecular Biology
Abstract
  • A defining feature of heterochromatin is methylation of Lys9 of histone H3 (H3K9me), a binding site for heterochromatin protein 1 (HP1). Although H3K9 methyltransferases and HP1 are necessary for proper heterochromatin structure, the specific contribution of H3K9 to heterochromatin function and animal development is unknown. Using our recently developed platform to engineer histone genes in Drosophila, we generated H3K9R mutant flies, separating the functions of H3K9 and nonhistone substrates of H3K9 methyltransferases. Nucleosome occupancy and HP1a binding at pericentromeric heterochromatin are markedly decreased in H3K9R mutants. Despite these changes in chromosome architecture, a small percentage of H3K9R mutants complete development. Consistent with this result, expression of most protein-coding genes, including those within heterochromatin, is similar between H3K9R and controls. In contrast, H3K9R mutants exhibit increased open chromatin and transcription from piRNA clusters and transposons, resulting in transposon mobilization. Hence, transposon silencing is a major developmental function of H3K9.
Date of publication
Identifier
  • doi:10.1101/gad.286278.116
Resource type
  • Article
Rights statement
  • In Copyright
Journal title
  • Genes & Development
Journal volume
  • 30
Journal issue
  • 16
Page start
  • 1866
Page end
  • 1880
Language
  • English
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