Journal
GENES & DEVELOPMENT
Volume 16, Issue 4, Pages 503-517Publisher
COLD SPRING HARBOR LAB PRESS
DOI: 10.1101/gad.952302
Keywords
lin-35; retinoblastoma; fizzy related; fzr-1; C. elegans; hyperproliferation; synthetic screen
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Funding
- NCI NIH HHS [P30 CA046934] Funding Source: Medline
- NIGMS NIH HHS [F32GM20029-01, R01 GM047869, GM37869, F32 GM020029] Funding Source: Medline
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We report here a synthetic-lethal screen in Caenorhabditis elegans that overcomes a number of obstacles associated with the analysis of functionally redundant genes. Using this approach, we have identified mutations that synthetically interact with lin-35/Rb, a SynMuv gene and the sole member of the Rb/pocket protein family in C. elegans. Unlike the original SynMuv screens, our approach is completely nonbiased and can theoretically be applied to any situation in which a mutation fails to produce a detectable phenotype. From this screen we have identified fzr-1, a gene that synthetically interacts with lin-35 to produce global defects in cell proliferation control. fzr-1 encodes the C. elegans homolog of Cdh1/Hct1/FZR, a gene product shown in other systems to regulate the APC cyclosome. We have also uncovered genetic interactions between fzr-1 and a subset of class B SynMuv genes, and between lin-35 and the putative SCF regulator lin-23. We propose that lin-35, fzr-1, and lin-23 function redundantly to control cell cycle progression through the regulation of cyclin levels.
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