Rare altered-function mutations in any of the interacting genes
unc-93,
sup-9, or
sup-10 result in the abnormal regulation or coordination of muscle contraction. These mutants display sluggish movement, are unable to lay eggs, and exhibit a characteristic rubber-band phenotype (when worms are prodded on the head, they contract and relax without moving backwards) (1,2,3). Loss-of-function mutations in any of these three genes completely suppress a rubber-band mutation in any of the three genes, suggesting that all three act at the same step, possibly as subunits of a protein complex(1). Two additional genes have been identified through reversion screens of rubber-band mutants: loss-of-function
sup-18 alleles completely suppress the rubber-band phenotype caused by
sup-10(
n983) while only partially suppressing the effects of
unc-93(
e1500) and
sup-9(
n1550) rubber-band alleles(2); rare
sup-11 alleles were isolated as dominant suppressors of
unc-93(
e1500) and act as recessive, partial suppressors of
sup-9 and
sup-10 rubber-band alleles. Both
unc-93 and
sup-10 have been cloned.
unc-93 encodes a novel, putative transmembrane protein(4).
sup-10 also encodes a novel protein (C. Cummins, J. Levin, H. R. Horvitz and P. Anderson, unpublished results). Cloning
sup-9 may provide new insights into the function of these interacting genes, especially since extensive genetic analysis of rubber-band mutants has yielded over 70 alleles of this gene, including loss-of-function, partial loss-of-function, and dominant-negative alleles. We are using transposon-tagged alleles of
sup-9 isolated as suppressors of
unc-93(
e1500) to clone this gene. 1. Greenwald, I. and H.R. Horvitz (1980). Genetics 96, 147-164. 2. Greenwald, I. and H.R. Horvitz (1986). Genetics 113, 63-72. 3. Levin, J. and H. R. Horvitz (1992). Genetics 135, 53-70. 4. Levin, J. and H. R. Horvitz (1992). Journal of Cell Biology 117, 143-155.