Worm Breeder's Gazette 8(2): 4
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.
I have conducted a search for dominant feminizing mutations. This was done by looking for F1 XX females amongst the self progeny of EMS- mutagenized N2 hermaphrodites. Females are distinguishable from hermaphrodites because they do not contain fertilized eggs, and their unfertilized oocytes build up in stacks along the proximal arms of the gonad, giving their bellies a striped appearance. So far, out of approximately 50,000 F1 animals screened 3 different kinds of mutants have appeared. First, a single allele of a mutation that has a dominant fer phenotype in which sperm appear not to develop beyond the 1 spermatocyte stage. Second, four dominant (gain-of- function) alleles of tra-1, which produce XX females and XO intersexes as heterozygotes with wildtype. Third, six dominant alleles of tra-2 ( briefly described at the worm meeting). These are unlike the tra-1( dom) mutations in that, although they make XX animals female when homozygous or heterozygous with wildtype, they do not appear to affect XO animals, which are male. Another property of these mutations is that the phenotype of XX animals is affected if the mutations are in trans with a putative null allele of tra-2, e1095 (which is an incomplete male as an XX homozygote). Depending on which dominant allele is used, the dom/null heterozygotes are self fertile intersexes (4 alleles), hermaphrodites (one putative allele) or female (one putative allele). I have recently obtained at least four independent loss-of-function mutations in one of these tra-2(dom) alleles (e1940) which show a recessive Tra phenotype and fail to complement tra-2. These prove that e1940 is indeed a mutation in tra-2, and it is likely that the other 5 dominant alleles are too, as they map in the right place and show the above mentioned phenotypes in trans with the recessive tra-2 allele. The sex specificity of these tra-2(dom) mutations is interesting because it suggests that, although tra-2 is supposedly active in the XX animal, its activity is normally modulated to allow spermatogenesis to occur, giving a hermaphrodite. These mutations appear to be eliminating or altering the susceptibility of tra-2 to whatever it is that modulates its activity. What turns tra-2 off in XX animals? I am in the process of looking for dominant suppressors of these tra-2(dom) mutations. In addition to the recessive tra-2 alleles mentioned, I have found 5 other revertants which may be extragenic and are being sorted out; these are hopefully mutations in genes that are involved in regulating tra-2.The screen utilizing the LGII balancer C1 is the same as above except that the screening strain is lin-2(e1309); 0)/ C1,dpy-10( e128)unc-52(e444). This allows us to identify immediately maternal effect lethals linked to chromosome II and balanced by C1. Of 4500 F1's screened thus far, 24 chromosome II maternal effect lethal mutations have been identified. They fall into 16 to 18 complementation groups (two have yet to be tested) and are evenly distributed over the balanced portion of LG II. Six are allelic to previously identified maternal effect lethal mutations in three genes ( we recovered four new alleles at the zyg-9 locus). Preliminary analysis indicates that there is a reasonable mix of strict and partial maternal effects among the mutants, and that complementing alleles show distinguishable phenotypes.