Worm Breeder's Gazette 16(3): 22 (June 1, 2000)

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

vex-2 may encode a transcriptional regulator that controls vulval development

David Garbe, Meera Sundaram

University of Pennsylvania School of Medicine, Philadelphia PA 19104

We identified a mutation, ku233, that causes defects in the first vulval specific division and thus named this locus vex-2 for vulval execution defective. In vex-2(ku233) hermaphrodites, the P(5-7).pxx cells often have abnormal nuclear morphology and spacing, and give rise to grossly abnormal progeny cells that form a disorganized invagination. At the dissecting scope level, ku233 hermaphrodites display incompletely penetrant egg laying defective, protruding vulva and sterile phenotypes, while ku233 males have crumpled spicules. We mapped ku233 to a small interval of chromosome III and rescued it with a single gene that encodes a possible transcriptional regulator. GFP reporter studies suggest that the gene product is expressed in many cells (including vulval cells) and that it localizes to the nucleus. RNAi against this candidate gene causes protruding vulva and sterile phenotypes, consistent with this gene being vex-2. However, the RNAi animals appear sicker than ku233 mutants and have several new phenotypes such as seam cell defects, gonadal defects and a partial vulvaless phenotype. Furthermore, although we have sequenced the entire coding region of our candidate gene, we have not yet found a lesion in ku233 mutants. We are performing a non-complementation screen to search for new alleles in order to resolve this issue.