Worm Breeder's Gazette 13(3): 103 (June 1, 1994)
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.
The sur-2 gene is the most mutable locus identified in a screen for suppressors of a let-60 ras gain of function allele( nl046 ).The sur-2 gene is currently defined by eight mutations that map 1 map unit away from unc-54 on IR. Each of the eight alleles completely suppresses the Multivulva phenotype of let-60 ( nl046 ).Seven of the eight alleles display a completely penetrant egg laying defect (Egl) while one allele is partially Egl. The Egl defect can be explained by an abberant vulval lineage. Although the vulval lineages vary, the most common defect is the induction of P6 .pto form a primary lineage while P5 .pand P7 .premain syncicial. In addition to the vulval defect, sur-2 mutants display other pleiotropic defects including a partial larval lethality, a partial dauer constitutive phenotype, gonad abnormalities and a male mating defect, suggesting that this gene is likely to play a key role in a number of important developmental decisions. The sur-2 ( ku9 )allele is likely hypomorphic because vulval induction is reduced when ku9 is placed over a deficiency. The sur-2 ( ku9 )allele is also able to suppress the Muv phenotype of lin-15 ( n765 )suggesting that sur-2 acts downstream of, or parallel to, let-60 and lin-15 .The interaction between sur-2 ( ku9 )and lin-1 is more difficult to interpret: the double mutant is extremely sick and most worms are sterile; however there is a partial suppression of the lin-1 Muv phenotype suggesting that sur-2 ,like lin-1 acts very downstream in the pathway.
The sur-2 gene was cloned by deficiency mapping and DNA-mediated transformation. Rescue of the ku9 egg laying defect requires nearly 14kb of genomic DNA. Developmental Northern blot analysis showed that the transcript is enriched during early embryonic and L1 stages of development. cDNA libraries constructed from these stages (Ahringer and Kimble) were screened and corresponding cDNA clones were obtained. DNA sequencing of the 14kb of genomic DNA and partial sequencing of the cDNAs indicate that sur-2 encodes a novel protein; thus our genetic screen has enabled us to identify a new member of the ras signalling pathway that has eluded biochemical investigation. Further genetic and molecular analysis of sur-2 is in progress.