Worm Breeder's Gazette 13(5): 49 (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.
Department of Molecular and Cell Biology, University of California Berkeley, CA 94720
We have been mapping and characterizing mutations identified in a clonal Nomarski screen for mutants with misplaced HSNs. One complementation group consists of four mutations: gm86 and gm88, which result in L1 arrest, and gm39 and gmll9, which are presumably hypomorphic alleles since mutants from this latter class are viable and have less severe cell migration defects. The HSNs were examined in gm39 adults using anti-serotonin staining. HSN cell bodies migrate 59percent of the normal distance (n=200). Besides the effects on HSN axons which we usually see in mutants with misplaced cell bodies, the axons look grossly normal. All four mutations affect a number of cell migrations besides the HSNs, including the CANs, ALMs, and coelomocytes. Mutants which survive to adulthood also have protruding vulvae and defects in distal tip cell migration. The most striking phenotype displayed by these mutants is a dorsal "notched head" deformity that is fully penetrant in gm86 and gm88 animals, and less so in gm39 and gm119. The head defect does not cause gm86 and gm88 lethality because notched head gm39 and gm119 animals often survive to adulthood. There are other mutants that have both cell migration defects and the notched head phenotype. Andrew Chisholm has found that vab-3 has distal tip cell migration defects (WBG 11.4, p. 83), and Fred Wolf in our lab has noticed that mig-10 has a low-penetrance notched head phenotype. Unfortunately, a screen through previously identified notched head vab mutants provided by the CGC and the MRC failed to find other mutants with HSN defects, with the exception of e64, which had slightly misplaced HSNs. gm86 maps to a 0.3 map unit interval on chromosome III, between lin-12 and ced-7. Since this region has been sequenced, we took a candidate gene approach, focusing on the alpha integrin subunit F54G8.3 because integrins are thought to play important roles in cell migration and morphogenesis. Preliminary injection experiments show that the F54G8 cosmid rescues the gm86 mutant phenotype. We are now injecting subclones of F54G8 to determine which gene on the cosmid is responsible for the rescuing activity.