Worm Breeder's Gazette 5(1): 8
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.
We have been studying unc-93 III, a muscle mutant that reverts spontaneously (Newsletter, January 1979). We have analyzed over 120 spontaneous and mutagen-induced revertants and have found that they define three sites, two extragenic (sup-9 II and sup-10 X) and one intragenic (within .01%). These studies have suggested that, although the e1500 mutation confers a striking phenotype, the phenotype that results from complete elimination of unc-93 gene product is wild-type. This hypothesis was originally based on three observations. (1) Intragenic revertants are obtained after EMS treatment at a frequency of about 4 x 10+E4, which is the frequency at which mutations due to complete elimination of gene function arise in wild-type animals after EMS mutagenesis (Brenner, 1974). (2) Only two visible alleles of unc- 93 have been detected (Nancy Tsung in this laboratory recently isolated n200, which is similar in phenotype to e1500 but weaker); thus, mutations in unc-93 that result in a detectable phenotype may be rare. (3) All of the intragenic revertants are recessive, suggesting that they do not simply restore gene function: e1500/+ is essentially wild-type in phenotype, whereas heterozygotes for these intragenic revertants are uncoordinated and egg-laying defective. Additional evidence now supports this model. Like e1500/intragenic revertant, e1500/Df(unc-93) is uncoordinated and egg-laying defective; thus, intragenic revertants are genetically equivalent to deficiencies of unc-93, which are null alleles by definition. We have also identified an intragenic revertant that is suppressed by sup-7(st5) X (a null allele suppressor; R. Waterston, personal communication) to restore the mutant phenotype. The two extragenic suppressors, sup-9 II and sup-10 X, are recessive and also arise with a frequency of about 4 x 10+E4; they also appear to represent complete elimination of gene function and are candidates for regulatory loci. Both of these fail to complement deficiencies for suppressor activity. Studies with the null allele suppressor sup-5(e1464) III (Waterston and Brenner, 1978) are in progress. [See Figure 1]