The purpose of this survey was to see if any of the egl mutants had abnormal male phenotypes, and to find out what proportion of a random sample of mutations isolated on the basis of a sex-limited phenotype were wholly sex-specific in their effects. A number of egl mutations turned out to cause abnormal male phenotypes, described below. Out of a total of 42 egl mutations inspected, only 12 appeared to have no phenotype outside of the egglaying system, and may define genes with roles confined to the hermaphrodite sex. However, for most of the loci analyzed, the null phenotype was undefined, so any conclusions regarding sex-specificity are tentative. Some male phenotypes had been described previously ( Trent et al., 1983; Desai and Horvitz, 1989); my observations confirm theirs. egl mutations of 26 loci had no discernible male phenotype: males appear wild-type and mate with ME of 2/3. Mutations of 6 loci (
egl-3,
egl-19,
egl-33 and
egl-39 ) had male mating defects which could be attributed to a non-sex- specific phenotype such as Unc;
egl-8 and
egl-30 males also have slight morphological defects. Mutations at 11 loci caused a male mating defect, apparently the result of morphological defects.
egl-5 and
egl-27 have grossly abnormal male tails as a result of abnormal tail lineages. The
egl-31 mutation causes abnormal M lineages in both sexes.
egl-8,
egl-20,
egl-34 and
egl-45 males all have variable morphogenetic defects in the tail.
egl-28 and
egl-32 males have gonad defects.
egl-2 males have abnormal bursal morphology, but this may result from a muscular or neural defect. egl mutations of 3 loci caused a male mating defect for no apparent reason.
egl-4, pear morphologically normal but mate very poorly. It is possible that there is some subtle defect in male mating which I have not noticed, or possibly a defect in male sperm function.
egl-41 males have slightly reduced mating efficiency, presumably the result of the weak feminization of
egl-41 XOs. Abnormal male phenotypes
egl-2 Males are well-coordinated and can back and turn, but cannot locate the vulva on hermaphrodites. The structures of the tail are all present and morphologically normal, but the cloacal structures ( including hook, spicules and gubernaculum) are permanently protruding in the position normally only seen during copulation. The hook and its sensillum are almost essential for vulval location (WBG 7,2) and it is possible that in these priapic worms the hook cannot operate properly.
n693 is semidominant for this phenotype:
n693/+ males mate reasonably well, but a small fraction have extruded cloacas. In a preliminary experiment the mating defect was rescued by exogenous imipramine.
egl-8 Males are Unc and slightly thin, and about one third have morphological defects in the fan: rays may be missing and the posterior fan may bulge out ventrally. Some males are quite severely affected.
egl-14 Males could back and turn in mating, but appeared to locate the vulva very poorly.
egl-18 Males have variable tail fan morphological abnormalities: rays may be blobby, misshapen or lost altogether. There is also a low penetrance Vab phenotype, both sexes.
egl-20 At 20 C and 25 C
n585 males have slightly abnormal tail morphogenesis (blobby rays, small fan) and variable defects in their sex muscles. Often the more anterior diagonal muscles appear to be missing or misplaced; sometimes ectopic diagonal-like muscles can be seen attaching in the midbody or more anteriorly. Some males have the crumpled spicules characteristic of sex muscle defects, although the other sex muscles appear to be present. In some animals the dorsal coelomocyte could not be seen. Occasionally the first ray appeared not to have migrated posteriorly, causing the alae to have a gap or end anteriorly to normal.
egl-27 There are several interesting phenotypes in
egl-27 mutants; I hope to describe the male lineage defects in detail at some time in the future.
egl-28 Male tail morphology is mostly wild-type, although a small fraction of males have minor morphogenetic defects (such as a small fan). In some
egl-28 males the germline has an unusual appearance: some sperm appear to be made initially, but the germ-line more distal to the sperm has a dough-like appearance and does not appear to be differentiating into sperm. This phenotype has low penetrance at 20 C and 25 C.
egl-32 Male tail morphology was wild-type, but variable abnormalities in male somatic gonads and germline were seen. These defects are incompletely penetrant. At 20 C, 4/67 males had abortive somatic gonad development, in which the gonad ended up as a structureless mass instead of a reflexed tube. Some sperm could be seen differentiating in the blob. 15/67 had germlines of abnormal appearance. At 25 C, 1/40 had the severe gonad defect and 12/40 had germline abnormalities. In 2 of the 12, gametes with the morphology of oocytes were seen. Neither the gonad nor the germline phenotype was seen in 79
egl-32 males grown at 15 C. These phenotypes are reminiscent of those described for
fog-1. Alleles of
fog-1 can cause feminization of the germline in both sexes, and have poorly understood effects on the male somatic gonad at low penetrance (T. Doniach, pc).
egl-32 may have functions similar to those of
fog-1,
n155 being a weak allele with a minor effect on the hermaphrodite germline giving the Egl phenotype. Alternatively, since
egl-32 and
fog-1 are linked, there may be a weak allele of
fog-1 in the strain; I have not tried to check this.
egl-34 Males are variably morpho-mab, some having blobby rays and some a misshapen ventral bursa: the hook can appear displaced anteriorly from the cloaca. Variable sex muscle defects also occur: some males have crumpled spicules, and occasionally some diagonal muscles are missing.
egl-35 At 25 C males appear variably morpho-mab (misplaced rays, swollen bursa) and occasionally have crumpled spicules. This defect is weaker at 20 C.
egl-45 Males are variably morpho-mab: some appear almost WT, while some have posterior bulges in the fan similar to those seen in
mab-9 males. Some have crumpled or missing spicules and very variable sex muscle defects. [See Figure 1]