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HIS-24 linker histone and SIR-2.1 deacetylase induce H3K27me3 in the Caenorhabditis elegans germ line.
Wirth, Martina; Paap, Franziska; Fischle, Wolfgang; Wenzel, Dirk; Agafonov, Dmitry E; Samatov, Timur R; Wisniewski, Jacek R; Jedrusik-Bode, Monika.
Afiliação
  • Wirth M; Max Planck Institute for Biophysical Chemistry, Laboratory of Chromatin Biochemistry, Am Fassberg 11, D-37077 Göttingen, Germany.
Mol Cell Biol ; 29(13): 3700-9, 2009 Jul.
Article em En | MEDLINE | ID: mdl-19380489
ABSTRACT
HIS-24 linker histone and SIR-2.1 deacetylase are involved in chromatin silencing in Caenorhabditis elegans. Depletion of SIR-2.1 results in cytoplasmic retention of HIS-24 in oocytes. However, the molecular working mechanisms of HIS-24 and SIR-2.1 are unclear. We show here a synergistic function of SIR-2.1 and HIS-24 that are together essential for maintenance of the H3K27me3 mark in the germ line of C. elegans. We demonstrate the synthetic effects of the two factors on brood size, embryogenesis, and fertility. SIR-2.1 and HIS-24 associate with the subtelomeric regions but apparently do not interact directly. We report that SIR-2.1 deacetylates H3K9 at subtelomeric regions and suggest that deacetylation of H3K9 is a prerequisite for H3K27 methylation. In turn, we found that HIS-24 specifically interacts with the histone H3 K27 region, when unmodified or in the trimethylated state. Overall, our data indicate that SIR-2.1 and HIS-24 contribute to the propagation of a specialized chromatin state at the subtelomeric regions and elsewhere in the genome.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Histonas / Caenorhabditis elegans / Proteínas de Caenorhabditis elegans / Sirtuínas / Células Germinativas Limite: Animals / Humans Idioma: En Ano de publicação: 2009 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Histonas / Caenorhabditis elegans / Proteínas de Caenorhabditis elegans / Sirtuínas / Células Germinativas Limite: Animals / Humans Idioma: En Ano de publicação: 2009 Tipo de documento: Article