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Genetics, Vol. 167, 1177-1185, July 2004, Copyright © 2004
doi:10.1534/genetics.103.024554
lin-35/Rb Cooperates With the SWI/SNF Complex to Control Caenorhabditis elegans Larval Development
Mingxue Cui*,
David S. Fay
and
Min Han*,1
* Howard Hughes Medical Institute and Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, Colorado 80309
Department of Molecular Biology, University of Wyoming, Laramie, Wyoming 82071
1 Corresponding author: Department of Molecular, Cellular, and Developmental Biology, Box 347, University of Colorado, Boulder, CO 80309-0347.
E-mail: mhan{at}colorado.edu
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.
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