C. elegans Rb NuRD and Ras regulate lin-39-mediated cell fusion during vulval fate specification

Zhe Chen, Min Han

Research output: Contribution to journalArticlepeer-review

43 Scopus citations


The tumor suppressor Rb and the NuRD (nucleosome remodeling and histone deacetylation) complex have been implicated in transcriptional repression during cell cycle progression and cell fate specification [1 2]. The Rb/E2F complex physically interacts with and thus recruits the NuRD complex to actively repress transcription [3-7]. Caenorhabditis elegans counterparts of Rb E2F/DP and some NuRD complex components appear to function in a common class B synthetic Multivulva (synMuv) pathway to antagonize RTK/Ras signaling during vulval fate specification [8-11]. Therefore it has been suggested that they function together in a single complex to repress vulva-specific gene transcription [8 9 11]. However little is known about the in vivo interactions between these class B synMuv genes and their relationships with other pathways in specific cellular processes during vulval development. We show that C. elegans Rb/E2F and NuRD complexes antagonize Ras activity by controlling a lin-39 Hox-mediated cell fusion event that regulates the competence of vulval cells. Interestingly Rb/E2F and NuRD complexes exhibit very different genetic properties. While the NuRD complex negatively regulates lin-39 Hox activity likely by downregulating its expression RB/E2F appears to play dual roles in regulating lin-39: a negative role in controlling its activity and a previously uncharacterized positive role in regulating its expression.

Original languageEnglish (US)
Pages (from-to)1874-1879
Number of pages6
JournalCurrent Biology
Issue number23
StatePublished - Nov 27 2001
Externally publishedYes

Bibliographical note

Funding Information:
We thank J. Simske and J. Harding for providing the jam-1::gfp construct, C. Kenyon for the lin-39::lacZ-integrated strain, D. Fay for RNAi constructs, and the C. elegans Genetic Center (University of Minnesota) for some strains used in this work. We also thank D. Starr, W. Johnson, D. Fay, C. Byars, and W. Wood for critically reading the manuscript. This work was supported by a RO1 grant from the National Institutes of Health (GM47869) to M.H., who is an Assistant Investigator of the HHMI.


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