Worm Breeder's Gazette 8(2): 9
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.
Adult vab-8(e1017)V worms have an apparently normal anterior, but their posterior half is thin, pale, and uncoordinated. This phenotype apparently results from misplacement of the two canal-associated (CAN) cells. During morphogenesis in wild-type embryos, the CAN cells migrate from the head region to bilaterally symmetric positions midway along the posterior excretory canals in the newly hatched L1, where they remain throughout postembryonic development. In vab-8(e1017) animals, the CAN cells usually fail to migrate and remain in the head ( Sulston and Hodgkin, Newsletter vol. 5, No. 1, p. 19; Sulston et. al., Dev. Biol. 100). By three-factor crosses we have mapped vab-8(e1017) to the right of sma-1 and the left of sqt-3. To learn more about the role of the vab- 8 gene in development and specifically in CAN cell migration, we are isolating and characterizing new vab-8 alleles. We have screened approximately 10,000 EMS-mutagenized chromosomes for mutations that fail to complement e1017 and have isolated one possible new allele whose phenotype in the dissecting microscope is indistinguishable from that of e1017. The e1017 allele is not suppressible by sup-7; we are currently testing suppressibility of the possible new allele. The relatively low frequency of vab-8 alleles in our complementation screen made us wonder whether an animal of genotype vab-8(e1017)/vab-8( null) might have a lethal phenotype which would preclude its isolation. To test this possibility, we have isolated a gamma-ray-induced deficiency, designated ctDf1, that fails to complement vab-8 and two flanking markers, sma-1 and sqt-3 [See Figure 1]. The deficiency complements unc-42 and lin-25 mutations and is homozygous lethal. Complementation of the actin genes, daf-11, and eql-10 is being tested. The phenotype of e1017/ctDf1 is indistinguishable from that of e1017/e1017 in the dissecting microscope. This suggests that e1017 is a allele of vab-8 and indicates that the low frequency of new mutant vab-8 alleles in our screen probably results from some property of the gene itself. We are currently looking for more EMS-induced vab-8 alleles using complementation screens with both e1017 and ctDf1. We will also explore the use of mutagens other than EMS.