Worm Breeder's Gazette 11(4): 100
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.
Two alleles of the gene lin-32, e1926 and u282, have been isolated by Kenyon and Hedgecock (1) and Chalfie and Au (2) respectively. Recently, another allele of lin-32, bx46, was isolated in our lab in a screen for Mab (male abnormal) mutations. The phenotype of a lin-32 mutant is loss of both V-rays and T-rays in the male. We do not believe any of the three alleles of lin-32 is a null, because none are completely expressive and because strong alleles of lin-32, which are also touch insensitive, are rare (2). lin-32(u282) is the strongest allele: about 90% of the males lack all the rays. We plan to isolate more alleles of lin-32 by a non-complementation screen in order to determine the null phenotype . Lineage analysis has been done on lin-32(e1926) by Kenyon and Hedgecock (1). They found that lin-32(e1926) caused the Q, postdeirid, and ray neuroblast cells to adopt certain hypodermal fates and suggested that lin-32 functioned in a switch between certain hypodermal and neuronal cell fates. Mutation in the gene lin-22 has the opposite effect (3). In males, it causes certain hypodermal cells to adopt neuroblast cell fates and produce ectopic postdeirids and rays. Rays arise from expression of the ray sublineage, and the posterior daughter of the ray precursor cell, Rn.p, does not make alae. Hence, lin-22 males lack alae. We constructed a lin-22(mu2);lin-32( u282) double mutant and found that, in double mutant males, lin-32 was epistatic to lin-22 in blocking the formation of ectopic postdeirids and rays, as pointed out previously by Kenyon and Hedgecock (1). Therefore, lin-32 appears to act downstream of lin-22 in generation of a neuroblast. If the lin-32 mutation only affected neuroblast cell fates, then we would expect to find neither rays nor alae in the lin- 22; utant. But interestingly, we found almost intact alae in double mutant males except at two or three broken points. One explanation for this phenotype is that the lin-32 mutation may not only affect neuroblast cell fates, but also certain hypodermal cell fates; it may transform the ectopic Rn.p cells produced in the lin-22 mutant from non-alae producing cells (tail seam cells?) into body seam cells. This effect of the lin-32 mutation in the lin-22 background is in contrast to its effect as a single mutant, where it does not affect hypodermal fates (lin-32 males do not have posterior alae, implying that Rn.p cells are not transformed to body seam cells). Alternatively, one or both of the daughter cells of Rn.a in lin-22;lin-32 double mutant may be transformed into body seam cells and produce alae. We are now following the cell divisions in the double mutant to characterize it further. We thank Duc Nguyen for isolating the bx46 allele.