Worm Breeder's Gazette 10(3): 88
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.
We have isolated four independent, EMS-induced mutations (bx25 bx26, bx29, and bx30) that affect the morphology of the sensory rays in C. elegans males. In males homozygous for these mutations, the sensory rays have an amorphous and somewhat lumpy morphology. This phenotype is distinct from the swollen ray phenotype of mab-7.One mutation, bx26, also exhibited a Dpy phenotype. This mutation has been mapped to dpy- 18 and fails to complement dpy-18(e1096). dpy-18(e1096) males also expressed the Mab phenotype described above. Because of these results, we have examined males homozygous for a variety of mutations that affect gross body morphology. [See Figure 1] Two of the mutations examined, dpy-11(e224) and sqt-1(e1350), exhibited the 'lumpy ray' phenotype. gross body morphology (Kusch and Edgar, Genetics 116: 621- 639, 1986), it is possible that these mutations represent null alleles of previously identified genes. This does not appear to be the case for bx25. This mutation maps to the left arm of linkage group IV, approximately 10 mu from dpy-9. No other mutations affecting gross body morphology have been mapped to this region of the genome. Based on these results, it appears that bx25, bx29, bx30, dpy-11, set of genes that are required for proper sensory ray morphogenesis during male tail development. The involvement of dpy-11, process indicates that ray morphogenesis is mediated, at least in part, by interactions between the fan cuticle and the sensory rays. bx25, bx29, and bx30 also may be mutations that primarily affect cuticular structure. Alternatively, these mutations may define genes that encode ray cell surface proteins required for interactions with the cuticle.