Sumoylation of LIN-1 promotes transcriptional repression and inhibition of vulval cell fates

Elizabeth R. Leight, Danielle Glossip, Kerry Kornfeld

Research output: Contribution to journalArticle

51 Scopus citations

Abstract

The LIN-1 ETS transcription factor inhibits vulval cell fates during Caenorhabditis elegans development. We demonstrate that LIN-1 interacts with UBC-9, a small ubiquitin-related modifier (SUMO) conjugating enzyme. This interaction is mediated by two consensus sumoylation motifs in LIN-1. Biochemical studies showed that LIN-1 is covalently modified by SUMO-1. ubc-9 and smo-1, the gene encoding SUMO-1, inhibit vulval cell fates and function at the level of lin-1, indicating that sumoylation promotes LIN-1 inhibition of valval cell fates. Sumoylation of LIN-1 promoted transcriptional repression and mediated an interaction with MEP-1, a protein previously shown to associate with the nucleosome remodeling and histone deacetylation (NuRD) transcriptional repression complex. Genetic studies showed that mep-1 inhibits vulval cell fates and functions at the level of lin-1. We propose that sumoylation of LIN-1 mediates an interaction with MEP-1 that contributes to transcriptional repression of genes that promote vulval cell fates. These studies identify a molecular mechanism for SUMO-mediated transcriptional repression.

Original languageEnglish
Pages (from-to)1047-1056
Number of pages10
JournalDevelopment
Volume132
Issue number5
DOIs
StatePublished - Mar 1 2005

Keywords

  • Chromatin
  • ETS
  • LIN-1
  • SUMO
  • Transcription
  • Vulval development

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