Worm Breeder's Gazette 11(4): 78
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.
Recessive mutations in any of six genes (smg-1 thru smg-6) result in the suppression of particular mutations in lin-29, unc-54, similarity is present in two cases where suppression has been examined at the molecular level: unc- 54, the body-wall muscle myosin heavy chain, and lin-29, a putative transcription factor required for the expression of adult seam cell fates. unc-54(r293) is a small deletion in the 3' untranslated region that removes the polyadenylation signal sequence. The result is a transcript aberrantly large in size, present in greatly reduced amounts. In unc-54(r293);smg double mutants, substantially more of the aberrant transcripts are present, presumably permitting sufficient unc-54 product to be synthesized for near-normal motility (Pulak and Anderson, WBG 11(1):54). However, lin-29(n546) is a point mutation in the translated region, converting and Arginine to an opal stop codon, and there does not appear to be a large difference in the size or abundance of lin-29 transcripts in n546 or the n546;smg double mutants vs. wild type ( Rougvie and Ambros, WBG 11(3) :37). Nevertheless, n546;smg double mutants show complete, allele-specific suppression of the lin-29 phenotype. This phenomenon may reflect a relatively subtle difference in lin-29 mRNA accumulation, perhaps due to instability potentiated by a paucity of ribosomes 3' of the opal stop codon. Numerous alternate explanations of the above results are possible, including that both unc-54(r293) and lin-29(n546) are suppressed at some other step in the transcript to product pathway, and that a process downstream of lin-29 action, but requiring n546 product, is stabilized. In order to address the burning question of what the smg genes really do, we are cloning smg-4 from the contig between her-1 and myo-3. We also request alleles of any cloned or about-to-be- cloned genes which show suppression or enhancement in the presence of smg mutations. It is worth checking mutants for smg-suppressibility, since it is often nice to have a homozygous mutant which can be maintained as nearly wild-type and because once the nature of smg- suppression is understood, it may shed light on the expression of suppressible genes as well.