Worm Breeder's Gazette 12(4): 40 (October 1, 1992)
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.
unc-73 ( e936 )animals have well-documented defects in the direction, and for some neurons, the extent of axon outgrowth (see Steven et al. abstract, this issue, for refs.). In addition, this strain shows, at a low penetrance, several phenotypes that are reminiscent of lin-17 ( n671 ):production of additional mec-3 -expressingcells, mispositioning of PVM between its normal position and the AVM region, and secondary vulval protrusions. These observations suggest that unc-73 might be involved in the general sensation by cells of direction within C. elegans, and reduction of its function could lead to defects in axon outgrowth, cell migration, and asymmetric cell division. This notion is supported by the identification of a region of homology between UNC-73 and yeast C dc24 p(Steven et al., this issue), which encodes an apparent guanine nucleotide exchange factor, and which is thought to control the sense of cell polarity within the yeast cell ( cdc24 mutants are defective in both knowing where to place the bud and where to extend when shmooing). We envision that unc-73 might be part of a signal transduction pathway that would communicate directional information from extracellular gradients or the matrix to the cell's interior.
To identify other genes in this pathway, we are pursuing two approaches. First, we have isolated non-Unc suppressors of unc-73 ( e936 ).Most of these appear to be intragenic, but two suppressors appear to be extragenic, dominant, and map somewhere on chromosome II. These suppressors have no striking phenotype on their own.
For a second approach, we sought to clone homologues of genes that interact with CDC24 . CDC42 is a member of the rho family of ras-like G proteins, and is a probable target of CDC24 .From the alignment of the yeast protein with a functional human CDC42 homologue, we designed degenerate oligonucleotides and PCR-amplified a ~700bp fragment. The sequence of each end of this fragment indicates that we probably have indeed cloned a C. elegans homologue of CDC42 .[See Figure]