Two genes,
fog-1 and
fog-3 , are essential to specify that germ cells differentiate as sperm rather than as oocytes. Several observations suggest that these genes might directly control sexual fate for germ cells. First,
fog-1 and
fog-3 are required in both sexes for the production of sperm rather than oocytes. Second, mutations in either gene are epistatic to alleles of other known sex determination genes. Third, mutations in these genes affect only germ cells. Fourth, sequence analysis suggests that
fog-3 is regulated by TRA-1A, which acts near the end of the sex-determination pathway. There are more than 60 known alleles of
fog-1, including two temperature sensitive alleles,
fog-1(
q253ts) and
fog-1(
oz15ts). Males that are homozygous for
fog-1(
q253ts) produce sperm at 15 degrees C and oocytes at 25 degrees C; hermaphrodites produce both sperm and oocytes at 15 degrees C and only oocytes at 25 degrees C, preventing self-fertilization. To identify genes whose products regulate or interact with FOG-1, we screened for suppressors of
fog-1(
q253ts). Such mutations might identify new genes that regulate sexual identity in germ cells. If they exist, we might also find mutations that bypass the need for
fog-1. So far, we have isolated 18 suppressor mutations after screening 40,000 haploid genomes, following exposure to ethyl methanesulfonate (EMS). The suppressed animals produce both sperm and oocytes at 25 degrees C, allowing self-fertilization. All the suppressors, except one, are recessive, and none are completely penetrant. Preliminary data indicate that most of these suppressors fall into two complementation groups. The alleles
v3,
v12,
v15,
v16 and
v21 fail to complement each other, and map in the vicinity of
rol-1 on LGII. Furthermore, the alleles
v7,
v8,
v9,
v17,
v18,
v20, and
v23 fail to complement, and map very near
unc-32 on LGIII. Finally, the alleles
v4,
q475, and
v11 complement both the sup on II and the sup on III, and so might identify additional genes. We are just beginning analysis of the remaining three suppressor mutations. The fact that suppressor alleles on LGIII are closely linked to
unc-32 suggested that they might be weak alleles of
mog-1. To test the possibility that these mutations on LGIII were novel alleles of
mog-1, we did complementation tests at both 15!C and 25!C using the
mog-1(
q223) mutation. All heterozygous F1 animals were fertile at both temperatures, suggesting that the suppressor alleles on LGIII might define a new locus. We are now using three factor mapping to localize these mutations more precisely, characterizing the phenotypes of the suppressors in the absence of
fog-1(
q253ts), and screening for additional alleles in a
mut-7 background.