Worm Breeder's Gazette 10(3): 90
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 an EMS-induced mutation, bx23, that specifically affects the development of sensory ray 6 in C. elegans males. In mutant individuals, the morphologically thickened ray 6 is missing, and in its place there is an ectopic ray that is located adjacent to, and is morphologically similar to ray 4. In most animals, the ectopic ray and ray 4 are fused on both sides. This phenotype is reflected in L4 males where the distinctive ray 6 papilla is missing and an ectopic papilla is present adjacent to the ray 4 papilla. bx23 does not affect male mating efficiency and no mutant phenotypes have been observed in bx23 hermaphrodites. The bx23 mutation has been mapped to approximately position +4.8 of linkage group X. No male specific defects have been described for any genes in this region. Thus, it appears that the bx23 mutation identifies a new gene that is required specifically for the differentiation of ray 6. The V6 cell lineage has not been determined in bx23 males, and therefore two simple explanations are possible to explain the mutant phenotype. First, it is possible that the V6 lineage is not affected by bx23. In this case, bx23 males would be defective in both the posterior migrations of the ray 6 precursor cell (R6) and its descendants, and in the differentiation of the ray 6 B neuron. Alternatively, a lineage defect could result in the failure of the R6 lineage and the recruitment of an ectopic ray from a different branch on the V6 lineage. For example, a ray cell group could be recruited from the anterior sister of the ray 4 precursor cell, V6.pppaa.