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.