The homeotic gene
mab-5is a member of the HOX family in nematodes. It was previously shown that in C. elegans (Cel) males it is important for migration of cells from specific lineages and for specification of tail structures.
mab-5 in hermaphrodites was found as egg laying competent, though the mutations increase the competence of P(7,8).p to adopt vulval fates (1,2) and in 15%of the mutants P(11,12).p cells fail to fuse (3). In contrast, in P. pacificus (Ppa)
mab-5 mutations leads to formation of posterior pseudovulvae in 75% of the hermaphrodites (4). Here we show that during organogenesis in
Ppa-mab-5 four bivulvae types are generated in 90% of the cases. In addition, we found that P(11,12).p fail to fuse in 15% of
Ppa-mab-5 mutant compared to 50% in
Cel-mab-5. On the basis of the findings summarized above we hypothesized that
Cel-mab-5 has a negative and redundant role in the pathway of vulval cell fate specification in posterior Pn.ps and that the loss-of-function mutation is predicted to show additional differentiated vulval structures. We indeed have found that 4% of
Cel-mab-5 hermaphrodites express posterior bivulvae phenotype similar to the
Ppa-mab-5vulval phenotypes. A gain of function mutation did not show any pseudovulva phenotypes. To understand further the nature of this previously undetected lf phenotype, we looked for cases in which posterior bivulvae are more frequent in Cel helping to reveal the nature of evolutionary diversity that appears to be present. For this we constructed a double mutant of
mab-5 with the fusion defective mutant
eff-1. 3ry sublineage Pn.p cells in
eff-1 frequently do not fuse and muv phenotype can be found in 2% of the cases. In the double mutant strain
mab-5;
eff-1 we have found a synergistic effect and the muv phenotype appeared in 55-60% of the animals. The most frequent source of these abnormal structures was P8.p, but other posterior Pn.p cells frequently divided and invaginated. Our findings suggest roles for
mab-5 in vulval formation. Specifically we argue that
mab-5 regulates posterior Pn.p vulval fate and interacts with
egl-5 in P(11,12).p specification. It appears that
mab-5 is not essential for vulva cell proliferation in contrast to the role of
lin-39 in this process. We intend to construct strains that will contain both the mutations and the cellular GFP markers of vulval fates, (
egl-17,
zmp-1) in order to find out the vulval fates adopted by the cells of the pseudovulva. In addition, we plan to check the double mutant of
mab-5 and
egl-5 in order to characterize the most posterior Pn.ps phenotype. (1)Cell, 1986, 46, 477-87 (2) Dev Biol. 1997, 182, 150-61. (3) Development, 2001, 128, 1793-804. (4) Curr Biol. 1998, 8,775-8.