Sister chromatid cohesion is fundamental to the faithful transmission of chromosomes during both meiosis and mitosis. The proteins involved in this process are highly conserved from yeast to human.
evl-14 mutants were identified in a screen for mutations causing abnormal eversion of the vulva (1). Similarly, an
scc-3 mutant with the protruding vulva and sterility phenotypes (Pvl Ste) was isolated in our screen. EVL-14 and SCC-3 are the only C. elegans homologues of the yeast sister chromatid cohesion proteins Pds5 and Scc3, respectively. Both
evl-14 and
scc-3 mutants displayed defects in the meiotic germline. In
evl-14 mutant animals, synaptonemal complexes (SCs) were detectable at the pachytene arrest, but more than six DAPI-positive structures were seen in diakinesis, suggesting that EVL-14/PDS-5 is important for the maintenance of sister chromatid cohesion in the late prophase. In
scc-3 mutant animals, SCs were not visible and ~24 DAPI- positive structures were seen in diakinesis, indicating that SCC-3 is necessary for the establishment of sister-chromatid cohesion. In budding yeast, Rec8 is a meiotic version of the cohesin subunit Scc1. C. elegans REC-8 is the likely worm ortholog of yeast Rec8 (2). Immunostaining using an anti-REC-8 antibody revealed that localization of REC-8 on chromosomes depends on SCC-3, but not EVL-14/PDS-5. To examine the possible roles of these proteins in early development, we carried out RNAi experiments.
evl-14 (RNAi) caused a range of phenotypes including embryonic lethality, larval lethality, the high incidence of males (Him) phenotype, and Pvl Ste. RNAi against
scc-3 gene produced 100% embryonic lethality. Also we found in both
evl-14 and
scc-3 mutants that vulval cells failed to divide. These results indicate that EVL-14/PDS-5 and SCC-3 have functions in mitosis, as well as meiosis in C. elegans. (1)Seydoux, G., Savage, C., and Greenwald, I. (1993). Devel. Biol. 157: 423-436. (2) Pasierbek, P., Jantsch, M., Melcher, M., Schleiffer, A., Schweizer, D., and Loidl, J. (2001). Genes Dev. 15:1349-1360.