Worm Breeder's Gazette 11(1): 51
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.
Ferguson and Horvitz (1985 Genetics 110: 17) have described five alleles of lin-15, all of which result in vulva-like protrusions on the ventral side of the mutant animals--referred to as the multivulva ( Muv) phenotype. The mutations are recessive to lin-15(+) and appear to result in reduced gene activity. Ferguson, Sternberg and Horvitz ( 1987 Nature 326: 259) showed that the vulval precursor cells (VPCs) P3. p-P8.p in lin-15 animals all express 1 and 2 fates. The latter authors also showed that laser ablation of the anchor cell in lin-15 animals did not abolish the Muv phenotype; they concluded from this result that the site of action of lin-15 was likely to be within the hypodermal VPCs and not in the anchor cell. (Muv mutations in other genes also appeared to be independent of the anchor cell signal.) One would thus expect that a mosaic animal in which lin-15(+) was present in the VPCs would be non-Muv, regardless of what other cells ( including the anchor cell) might be lin-15. My results contradict this simple prediction. Among about 7,000 zygotes of genotype unc-93(e1500) III; unc-3 09) sup-10(0) X; mnDp14(X;f) [unc-3(+) sup-10(+)], 15 animals were found that I concluded had suffered duplication loss at P1. These animals were non-Unc-93 non-Unc-3 and gave only Unc-3 geny. Seven of the 15 were checked for FITC staining and found to be non-Osm-1, as expected. The VPCs are descended from AB and thus should have contained lin-15(+). Ten of the 15 animals had 1-3 ventral protrusions at positions either anterior or posterior to the vulva. Many of the mosaics were thus unexpectedly Muv, although the number of protrusions per animal was generally less than that found for pure lin-15(n309) animals. Another class of non-Unc-93 non-Unc-3 animal among the same zygotes provided a kind of control. These gave some wild-type (as well as Unc-3 geny, indicating that their free duplications no longer carried sup-10(+). There were 15 of these animals, and none showed any ventral protrusions. It thus seems unlikely that many of the protrusions found in the mosaic animals could be attributed to weak dominance of the lin-15(+) gene on the free duplication or to frequent extra duplication loss in the lineages leading to the VPCs. I am in the process of constructing animals that should allow me to identify mosaics in which duplication loss occurred at AB or AB.p, ancestors of the VPCs. I would expect that such mosaics might also be Muv, i.e., that lin-15(+) is needed both for normal signal generation and for normal response to signal. (I should point out that Ferguson et al. stated explicitly that their results did not exclude this possibility.) I would also like to do additional work with the duplication-loss-at-P1 mosaics. First, I hope, in collaboration with Ed Hedgecock, to follow the lineages of VPC descendants in such animals. And second, I would like to see if ablation of the anchor cell in these animals would abolish their Muv-ness (since the result so far only points to an effect of one or more descendants of P1). I'd like to thank Paul Sternberg for encouraging me to generate these mosaics.