Worm Breeder's Gazette 5(2): 27
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.
In the last newsletter, we described genetic studies of the unc-93 locus and suggested that, although rare alleles of unc-93 such as e1500 confer a striking uncoordinated and egg-laying defective phenotype, the phenotype resulting from null alleles is wild-type. One possible and intriguing explanation for the wild-type null phenotype of unc-93 is that in the absence of the unc-93 pathway, an alternative pathway(s) still functions. A specific example of such redundancy is that another gene product may be able to substitute directly for the unc-93 product, i.e. unc-93 may be a member of a multigene family. The e1500 mutation, which is semidominant, may result in a product that is toxic; elimination of the toxic product restores the wild-type phenotype. The genetic property that originally attracted our attention spontaneous (intragenic) reversion ( see previous Newsletters)--may be an indicator of other genes with wild-type null phenotypes. For example, unc-58(e665) X ('shaker') reverts spontaneously, and experiments similar to those described for e1500 have indicated that the null phenotype of unc-58 is wild-type. Bob Waterston has informed us that unc-92(st15) V, which reverts spontaneously, may also have a wild-type null phenotype. The rate of spontaneous reversion (10 ) seen for e1500 and e665 probably reflects the normal rate of spontaneous mutagenesis. As other genes with wild-type null phenotypes are identified, some of the genetic strategies we have used for our analysis of unc-93 may be applicable. For example, we generated deficiencies of unc-93 and sup-9 (a recessive extragenic suppressor of e1500) by exploiting the observation that e1500/null is mutant: [See Figure 1] Many of the wild-type animals obtained using the above procedures were shown to harbor deficiencies by recessive lethality and by failure to complement neighboring markers (intragenic revertants and dominant suppressors of e1500 were distinguishable from deficiencies by these criteria). The map below shows the deficiencies of unc-93 we have generated. The protocol used for unc-93 deficiencies may be modified for more general applicability (i.e., for genes that are not also suppressed by extragenic suppressors): mutant males may be irradiated and directly mated with marked revertants hermaphrodites, or revertant males may be mated with irradiated mutant hermaphrodites. The protocol used for deficiencies of sup-9 may also be modified: irradiated mutant males may be mated with marked suppressed hermaphrodites, or suppressed males may be mated with irradiated mutant hermaphrodites. [See Figure 2]