Worm Breeder's Gazette 11(2): 113
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.
mab-19(bx38), an EMS-induced recessive mutation, results in the variable loss of the three T-derived sensilla, rays 7-9. Preliminary lineage data (presented in a poster at the worm meeting in May, 1989) suggest that only the male-specific divisions of T and its descendents are affected. bx38 does not affect the lineages of V5 or V6, from which the other six rays are derived. In the two animals we have observed, T.apap and T.appa or their descendants fail to divide. bx38 males are almost infertile, but we do not know if this is related to T ray loss. We have localized mab-19(bx38) to LGX between -3.2 and -1.5. We have found that all of the Dpy mutations tested to date suppress the Mab phenotype of bx38. On the other hand, Lon mutations, lon-1 ( e185) and lon-2(e678), enhance the Mab phenotype in double mutants. For example, lon-1; mab-19(bx38) males are missing rays 7-9 a larger percentage of the time. In addition, the tails of these animals are often severely deformed. The tails are rounded instead of tapered, the V5 and V6-derived rays do not fully extend, and some of the males have crumpled spicules. lon-2 utants show a similar, though less severe phenotype. The suppressor-enhancement data we have obtained to date are summarized in the following table: [See Figure 1] Phenotypic suppression in Dpy backgrounds has been found for glp-1 ( ts) alleles (Maine and Kimble, Development 103, 133-143, 1989) and bli- 6(mn4) (Winter and Herman, WBG 9:3). Suppression in both cases is allele-specific as well as gene-specific. Further, no Lon enhancement or suppression has been found in either case. While we have not tested the phenotypic effect on bx38 of all Dpy alleles or any Sqt, Sma, or Rol alleles, it appears that suppression of the Mab (bx38) phenotype by Dpy is more general than that seen for glp-1 or bli-6. One possibility is that precise cell-cell interactions are necessary for mab-19 wild-type function. Changes in body shape may alter cell interactions enough to affect the penetrance of the bx38 Mab phenotype. We are continuing our investigation of the effects of body shape on the phenotypic expression of mab-19(bx38). We have not investigated whether the Dpy suppression extends to the mating defect. Laser ablation experiments have shown that ablation of T or T.ap in bx38 animals phenocopies the deformed tail phenotype seen in lon-1 ( e185); mab-19(bx38) males. If the same ablations are performed on wild-type males, the resulting tails exhibit wild-type morphology (but no T-derived rays). One model consistent with these observations is that mab-19 is not expressed in the T lineage, and that one role of mab-19 in wild-type males is to signal those cells involved in the morphogenesis that takes place during L4 lethargus (see S. Emmons, WBG9:3 for a detailed description of this process). A second, similar signal is provided by T or its descendants. Neither of these signals is essential, but if both are missing, the males exhibit a rounded tail morphology. We plan to test this hypothesis by searching for synthetic mutations that result in both the morphogenetic defect and the bx38 Mab phenotype. According to this model, there must be cells receiving the putative signals. In an attempt to locate these cells, we have ablated V6.p and B.p in several bx38 animals, but we have not observed similar morphogenetic defects. Another type of suppression of the Mab (bx38) phenotype has been observed. If the animals enter the dauer pathway of development, the penetrance of the adult Mab phenotype of bx38 is lowered from 75% to about 10% (n = 2/24). Some heterochronic mutations, lin-4, suppressed when animals develop via the dauer pathway. Liu and Ambros have thus proposed that alternative genetic controls are employed when development proceeds via the dauer pathway (1987 CSH C. elegans meeting abstract, p. 127). An alternate dauer pathway for ray development and morphogensis is a model consistent with our data. One prediction of this model is that lon-1(e185);mab-19(bx38) animals that develop via the dauer pathway would not only be wild-type with respect to T-derived ray formation, but also with respect to the morphogenetic defect. We are currently testing this possibility.