Caenorhabditis Elegans EVL-14/PDS-5 And SCC-3 Are Essential For Sister Chromatid Cohesion In Meiosis And Mitosis

Sister chromatid cohesion is fundamental to the faithful transmission ofchromosomes during both meiosis and mitosis. The proteins involved in this processare highly conserved from yeast to human. evl-14 mutants were identified fromGreenwald lab in a screen for mutations causing abnormal eversion of the vulva.Similarly, an scc-3 mutant with the protruding vulva and sterility phenotypes wasisolated in a screen carried out in the Han laboratory. Here I reported positionalcloning and functional characterization of evl-14 and scc-3, which encode the likelysole C. elegans homologs of the yeast sister chromatid cohesion proteins Pds5 andScc3, respectively. Both evl-14 and scc-3 mutants displayed defects in the meiotic germline. In evl-14mutant animals, synaptonemal complexes (SCs) were detectable at the pachytenearrest, but more than the usual six DAPI-staining positive structures were seen indiakinesis, suggesting that EVL-14/PDS-5 is important for the maintenance of sisterchromatid cohesion in the late prophase. In scc-3 mutant animals, normal SCs werenot visible and ~24 DAPI-staining positive structures were seen in diakinesis,indicating that SCC-3 is necessary for the establishment or maintenance of sister-chromatid cohesion. In budding yeast, Rec8 is a meiotic version of the cohesinsubunit Scc1. C. elegans REC-8 is the likely worm ortholog of yeast Rec8.Immunostaining using an anti-REC-8 antibody revealed that localization of REC-8 onchromosomes depends on SCC-3, but not EVL-14/PDS-5. 1The possible roles of these proteins in early development were examined by meansof RNA interference (RNAi) experiments. evl-14 RNAi caused a range of phenotypesincluding embryonic lethality, larval lethality, the high incidence of males (Him),protruding vulva and sterility. RNAi against scc-3 gene produced 100% embryoniclethality. All of the examined scc-3 RNAi embryos displayed abnormal mitosis. AlsoI found that vulval cells and ventral uterine cells failed to divide in both evl-14 andscc-3 mutants. These results indicate that EVL-14/PDS-5 and SCC-3 have functionsin mitosis, as well as meiosis in C. elegans.