CGC Bibliography Paper 4998

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

Chen Z, Han M

Medline:
11728311
Citation:
Current Biology 11: 1874-1879 2001
Type:
ARTICLE
Genes:
dpl-1 efl-1 hda-1 let-23 let-60 let-341 lin-1 lin-3 lin-8 lin-15 lin-35 lin-37 lin-38 lin-39 lin-53 mab-5 mpk-1
Abstract:
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