The recessive mutation
mab-10(
e1248) II was identified by J. Hodgkin in his screen for male-infertile mutants (Genetics 103:43-64, 1983).
mab-10(
e1248) males have rather subtle bursal defects, are completely infertile, and have been reported to occasionally have supernumerary molts. I have extended these observations and find that
mab-10(
e1248) causes a highly penetrant, male-specific retarded heterochronic defect in addition to affecting bursal development. Age-synchronized 248); 90) males and hermaphrodites were followed from the L4/adult molt at 20 C. Male animals were found to synchronously begin a supernumerary molt 18-20 hrs after L4 lethargis. Hermaphrodites of the same age (n=32) were carefully observed under DIC optics and showed no signs of a supernumerary molt. The male-specific supernumerary molt phenotype was found to be highly penetrant (>95%) at 16 C, 20 C, and 25 C. The male supernumerary molt appears to result from the production of a second adult cuticle. Young (presupernumerary molt)
mab-10(
e1248) adult males appear to have normal 'first' adult cuticles, as judged by the presence of adult lateral alae and wild-type staining with WGA and Ab117. The supernumerary cuticles also have adult lateral alae. To my knowledge, none of the known retarded heterochronic mutations (e.g., in
lin-29, s pattern of adult supernumerary molts. The
mab-10(
e1248) supernumerary molt is not affected by passage through the dauer larvae stage. I have mapped
mab-10(
e1248) (scoring the supernumerary molt phenotype) to the right of the gene cluster on linkage group II, between
unc-4 and
rol-1 and near
lin-29. (Male infertility has co- segregated with the supernumerary molt phenotype in these mapping experiments.) Interestingly, this places
mab-10 in a region of the chromosome where the nearby known morphological mutations (in the genes
lin-29, ifically affect the adult cuticle (see figure).
mab-10(
e1248) is complemented by
lin-29 and the deficiencies mnDf87 and mnDf77, but not by the deficiencies mnDf89 or mnDf83. I have carefully observed the phenotype of mnDf89/mab-10
(e1248) heterozygous males and hermaphrodites, and find the same pattern of male specific supernumerary molts as seen in mab- 10
(e1248) homozygotes. This argues against the possibility that the male specificity of
mab-10(
e1248) results because this is a partial loss-of-function mutation and that a null mutation would affect both sexes. However, mnDf89/mab-10
(e1248) males have significantly more abnormal bursae than
mab-10(
e1248) homozygotes, suggesting that
mab-10(
e1248) is not a null mutation. (mnDf89/+ males are wild-type.) Because the bursal defects (and male infertility) of
mab-10(
e1248) are observed before the supernumerary molt, the relationship between these phenotypes is unclear. It is also not obvious why a heterochronic defect would appear to be so sex-specific. In this regard, it is interesting to note that neither retarded nor precocious heterochronic mutations affect the timing of expression of male- specific bursal surface markers (Link, Ehrenfels, and Wood, Development 103:485-495, 1988). Perhaps some portion of male or bursal development involves an independent temporal program. [See Figure 1]