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lin-35Rb cooperates with the SWISNF comp ... itis elegans larval development
lin-35/Rb cooperates with the SWI/SNF complex to control Caenorhabditis elegans larval development.
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Null mutations in lin-35, the Caenorhabditis elegans ortholog of the mammalian Rb protein, cause no obvious morphological defects. Using a genetic approach to identify genes that may function redundantly with lin-35, we have isolated a mutation in the C. elegans psa-1 gene. lin-35; psa-1 double mutants display severe developmental defects leading to early larval arrest and adult sterility. The psa-1 gene has previously been shown to encode a C. elegans homolog of yeast SWI3, a critical component of the SWI/SNF complex, and has been shown to regulate asymmetric cell divisions during C. elegans development. We observed strong genetic interactions between psa-1 and lin-35 as well as a subset of the class B synMuv genes that include lin-37 and lin-9. Loss-of-function mutations in lin-35, lin-37, and lin-9 strongly enhanced the defects of asymmetric T cell division associated with a psa-1 mutation. Our results suggest that LIN-35/Rb and a certain class B synMuv proteins collaborate with the SWI/SNF protein complex to regulate the T cell division as well as other events essential for larval growth.
Cui M, Fay DS, Han M
Genetics
2004-07-01 00:00
167
3
1177-85
Animals,Caenorhabditis elegans,Caenorhabditis elegans Proteins,Cell Lineage,Larva,Mutation,Nuclear Proteins,Phenotype,RNA Interference,Repressor Proteins,Saccharomyces cerevisiae Proteins,Trans-Activators,Caenorhabditis elegans Proteins,Nuclear Proteins,Repressor Proteins,Saccharomyces cerevisiae Proteins,Trans-Activators,lin-35 protein, C elegans,SWI3 protein, S cerevisiae
Howard Hughes Medical Institute and Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, Colorado 80309, USA
Genetics
NIGMS GM-47869
0016-6731
10.1534/genetics.103.024554
167/3/1177
535
True
15280233
