Worm Breeder's Gazette 13(5): 70 (February 1, 1995)
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.
IMBB, Simon Fraser University, Burnaby, BC, V5A 1S6 Many C. elegans genes that are required for specific postembryonic developmental decisions have a lethal null phenotype. For example, many lin-3/let-23 pathway genes and lag pathway genes are essential. To identify additional essential genes involved in development, we have begun a systematic screen of existing lethal mutants for those exhibiting postembryonic lineage defects. We have focused on the first asymmetric cell division of several postembryonic blast cells (lateral and ventral epidermis, somatic gonad, and male B and Y). These cells all divide early (L1 larval stage), and morphological differences between the two daughter cells are apparent immediately following cell division. Thus we can screen all lethal mutants that arrest after L1 for the disruption of these cell lineages. To date, we have screened 167 mutations representing 149 loci on LG III(left) and LG V(left) for asymmetric cell division defects. We have identified seven candidates; four are weakly (~50%) penetrant for a Lin phenotype, whereas three are strongly penetrant, including let-765 III, discussed below. let-765 is identified by a single mutation, s2575 (Stewart et al., WBG 13(4) 95). In s2575 homozygous males, the first division of the B cell is disrupted. In wild-type animals cytokinesis is unequal and the B.a daughter is larger than the B.p daughter, but in let-765 mutants the cells are of equal size. Some other asymmetric cell divisions are not affected by the let-765 mutation, as the initial Z1/Z4, Pn, and Vn cell divisions are normal. s2575 homozygous animals arrest in L2 stage, with no further cell division in the B lineage. Multipoint mapping has placed let-765 between sma-4 and unc-36, but to the left of sma-3. let-765 is uncovered by sDf127, and s2575/sDf127 animals arrest after hatching, but prior to postembryonic cell division. Thus, s2575 may not represent a null mutation in let-765. To better understand the function of let-765, we are currently trying to rescue the gene by testing cosmids in the region (Collins et al., WBG 13(4) 94). Once we obtain rescue, we will be able to use the cosmid transgene as a mini- duplication to recover additional alleles of let-765.