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Argonaute NRDE-3 and MBT domain protein LIN-61 redundantly recruit an H3K9me3 HMT to prevent embryonic lethality and transposon expression.
Padeken, Jan; Methot, Stephen; Zeller, Peter; Delaney, Colin E; Kalck, Veronique; Gasser, Susan M.
Afiliação
  • Padeken J; Friedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland.
  • Methot S; Friedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland.
  • Zeller P; Friedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland.
  • Delaney CE; Faculty of Natural Sciences, University of Basel, CH-4056 Basel, Switzerland.
  • Kalck V; Friedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland.
  • Gasser SM; Friedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland.
Genes Dev ; 35(1-2): 82-101, 2021 01 01.
Article em En | MEDLINE | ID: mdl-33303642
The establishment and maintenance of chromatin domains shape the epigenetic memory of a cell, with the methylation of histone H3 lysine 9 (H3K9me) defining transcriptionally silent heterochromatin. We show here that the C. elegans SET-25 (SUV39/G9a) histone methyltransferase (HMT), which catalyzes H3K9me1, me2 and me3, can establish repressed chromatin domains de novo, unlike the SETDB1 homolog MET-2. Thus, SET-25 is needed to silence novel insertions of RNA or DNA transposons, and repress tissue-specific genes de novo during development. We identify two partially redundant pathways that recruit SET-25 to its targets. One pathway requires LIN-61 (L3MBTL2), which uses its four MBT domains to bind the H3K9me2 deposited by MET-2. The second pathway functions independently of MET-2 and involves the somatic Argonaute NRDE-3 and small RNAs. This pathway targets primarily highly conserved RNA and DNA transposons. These redundant SET-25 targeting pathways (MET-2-LIN-61-SET-25 and NRDE-3-SET-25) ensure repression of intact transposons and de novo insertions, while MET-2 can act alone to repress simple and satellite repeats. Removal of both pathways in the met-2;nrde-3 double mutant leads to the loss of somatic H3K9me2 and me3 and the synergistic derepression of transposons in embryos, strongly elevating embryonic lethality.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Proteínas Cromossômicas não Histona / Elementos de DNA Transponíveis / Heterocromatina / Regulação da Expressão Gênica / Proteínas de Ligação a RNA / Caenorhabditis elegans / Proteínas de Caenorhabditis elegans Limite: Animals Idioma: En Ano de publicação: 2021 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Proteínas Cromossômicas não Histona / Elementos de DNA Transponíveis / Heterocromatina / Regulação da Expressão Gênica / Proteínas de Ligação a RNA / Caenorhabditis elegans / Proteínas de Caenorhabditis elegans Limite: Animals Idioma: En Ano de publicação: 2021 Tipo de documento: Article