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First published online 14 June 2006
doi: 10.1242/dev.02444

Development 133, 2695-2704 (2006)
Published by The Company of Biologists 2006
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C. elegans ISWI and NURF301 antagonize an Rb-like pathway in the determination of multiple cell fates

Erik C. Andersen, Xiaowei Lu* and H. Robert Horvitz{dagger}

Howard Hughes Medical Institute, Department of Biology, Room 68-425, MIT, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.

{dagger} Author for correspondence (e-mail: horvitz{at}mit.edu)

Accepted 15 May 2006

The class A, B and C synthetic multivulva (synMuv) genes act redundantly to negatively regulate the expression of vulval cell fates in Caenorhabditis elegans. The class B and C synMuv proteins include homologs of proteins that modulate chromatin and influence transcription in other organisms similar to members of the Myb-MuvB/dREAM, NuRD and Tip60/NuA4 complexes. To determine how these chromatin-remodeling activities negatively regulate the vulval cell-fate decision, we isolated a suppressor of the synMuv phenotype and found that the suppressor gene encodes the C. elegans homolog of Drosophila melanogaster ISWI. The C. elegans ISW-1 protein likely acts as part of a Nucleosome Remodeling Factor (NURF) complex with NURF-1, a nematode ortholog of NURF301, to promote the synMuv phenotype. isw-1 and nurf-1 mutations suppress both the synMuv phenotype and the multivulva phenotype caused by overactivation of the Ras pathway. Our data suggest that a NURF-like complex promotes the expression of vulval cell fates by antagonizing the transcriptional and chromatin-remodeling activities of complexes similar to Myb-MuvB/dREAM, NuRD and Tip60/NuA4. Because the phenotypes caused by a null mutation in the tumor-suppressor and class B synMuv gene lin-35 Rb and a gain-of-function mutation in let-60 Ras are suppressed by reduction of isw-1 function, NURF complex proteins might be effective targets for cancer therapy.

Key words: ISWI, NURF, Rb, Ras, C. elegans


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© The Company of Biologists Ltd 2006