Worm Breeder's Gazette 11(2): 103
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.
Mutations that affect the fates of cells in the vulval equivalence group are often divided into two classes: vulvaless (Vul) and multivulva (Muv). However, one can also distinguish them on the basis of their effects on the morphology of males. lin-2, lin-7, and lin-10 hermaphrodites are Vul and the males all have wild-type tail morphology. In contrast, the males of genotypes let-23(nonlethal reduced-function) and let-60(dominant Vul) /+, both with a Vul hermaphrodite phenotype, and lin-1, midominant), all Muv, are morphologically wild-type except for the spicules, which are short and crumpled. As a result, these mutants cannot mate. In wild-type, the B cell divides only in males to produce all of the cells which make up the spicules, as well as several proctodeal cells. The B lineage includes two 2-cell equivalence groups: Balpha/B (B.alaa and B.araa) and Bgamma/Bdelta(B.alpp and B.arpp). We have analyzed the B cell lineage in the mutant males to determine the lineage defects responsible for the morphological defect. Our observations indicate that these vulval genes are involved in decision making within the Balpha/B and Bgamma/Bdelta equivalence groups. Note that aside from the equivalence group abnormalities described below, the remaining divisions of the B cell in these mutants are essentially wild-type. The Vul mutants let-23(sy97) and let-60(sy95)/+ cause a transformation from Balpha to B [8/10 lineaged in let-23(sy97); 315 in let-60(sy95)/+]. For both B.alaa and B.araa the number and timing of divisions, and the relative position of the progeny cells, are B - like. This transformation is not solely responsible for the spicule defect, however, because adult mutants with wild-type lineage have spicules which are less deformed than transformed animals, but which are not wild-type. Since only the cell divisions, and not the cell deaths, were followed in the lineages, the additional defect could be due to an abnormality in cell death, spicule morphogenesis, or associated muscle or other tissue. The Muv mutants lin-1(e1777), 09), and lin-34( sy103) show a rare B to Balpha transformation [1/4 in lin-1(e1777); 1/6 in lin-34(sy103)] and an abnormality in the Bdelta lineage [5/5 in lin-1(e1777); 1/1 in lin-15(n309); 7/8 in lin-34(sy103)]. The B to Balpha transformation, like the opposite Balpha to B transformation in Vul mutants, results in both B.alaa and B.araa having the number and timing of divisions, and the relative positions of the progeny cells associated with Balpha. The Bdelta abnormality results from the two Bdelta progeny dividing to give two additional progeny. We hesitate, however, to call this a partial Bdelta to Bgamma transformation because the timing and axis of division remain Bdelta- like. Full Bdelta to Bgamma transformations have already been observed in lin-12 loss-of-function mutants [Greenwald et al., Cell 34:435-444(1983)], and it has been traditionally thought that lin-12 controls the Bgamma/Bdelta decision. Preliminary characterization of the interaction of these mutations has supplied another possible explanation for the Bdelta abnormality. Heterozygous let-60(dmVul)lin-34(sd) males are both wild-type in morphology and able to mate. These dominant mutations are able to suppress each other's phenotype in trans, providing another indication that these two classes of mutations, which map to the same genetic location, define genes that either interact very closely, or are indeed alleles of the same gene (see Han et al., this issue). As noted above, let-60 is essential for Balpha specification. lin-34 mutations, interpreted as causing hyperactivity of let-60 gene product, occasionally cause both B.alaa and B.araa to be Balpha-like. It is thus curious that the Bdelta abnormality approximates Balpha in the timing and axes of divisions and number of progeny cells. In Muv mutants, both Balpha and Bdelta divide left/right, and then each daughter divides (approximately) dorsal/ventral. Therefore, it is possible that Bdelta is transformed to Balpha by an inappropriately high level of let-60 activity in or on Bdelta. We hope that our further analysis will elucidate the nature of this lineage abnormality and the control of the Bdelta cell fate. Our data demonstrate that several genes important for cell interaction in the vulva are additionally essential for proper cell interaction in the male B cell lineage. Since there are vulval genes which have a male pleiotropy and other genes which do not, it is possible that the pleiotropic genes encode products that are components of a generalized cell interaction mechanism used throughout nematode development, including, but not restricted to, the two closely studied systems of the vulva and the male tail. Sulston and White [Dev. Biol. 78:577-597(1980)] demonstrated that within the Balpha/B equivalence group Balpha is 1 and B is 2 . In the vulva, the six vulval precursor cells (VPCs) make a fate decision between vulval tissue (1 , 2 ) and hypodermal tissue (3 ). Mutations in Vul genes result in all hermaphrodite VPCs and the male B.alaa and B.araa adopting lower fates (3 and 2 respectively). Conversely, mutations in Muv genes result in all VPCs and (rarely) both B.alaa and B.araa adopting higher fates (1 /2 and 1 , respectively). Thus, these genes are playing analogous roles in the specification of cell fate in the vulval and Ba/B equivalence groups. Since some genes are specific to the vulva, we expect there are other genes that are specific to the B lineage. Thus, in addition to establishing the epistasis of the spicule lineage defects among existing mutations, we are currently isolating new male tail mutants in order to identify genes which work before, at the same time, and after the cell equivalence group interaction regulated by this subset of vulval genes. [See Figure 1]