sup-9 is a member of a group of interacting genes (
unc-93,
sup-9,
sup-10, sup-ll, and
sup-18) involved in muscle structure and function.
unc-93(elS00) and sup-lO
(n983) are rare, altered-function mutations that confer a distinctive uncoordinated ('rubber-band'), muscle- defective phenotype. When a rubber-band mutant is prodded on its head, the worm contracts and then relaxes without moving backwards, while a wild-type worm simply moves backwards. The rubber-band phenotype suggests a defect in the regulation or coordination of muscle contraction. Null alleles of
unc-93,
sup-9,
sup-10, and
sup-18 result in a wild-type phenotype alone and are recessive suppressors of elS00 and
n983. Certain rare alleles of sup-ll act as dominant suppressors of elS00 and recessive suppressors of
n983; the sup-ll null phenotype is embryonic lethality. Our model for the interaction of these genes is that the rubber-band mutations produce abnormal gene products that disrupt a redundant process in the regulation of muscle contraction, but the absence of the gene products of any of these four genes does not adversely affect muscle contraction. A new rubber-band mutation, sup-9fnlSS0), causes a dominant uncoordinated phenotype and a recessive phenotype of extreme sluggishness, very slow growth, and the production of few, if any, progeny. Based on genetic mapping and the reversion of the Unc phenotype associated with nlSS0 resulting in cis-dominant
sup-9 null mutations, we have assigned nlSS0 as an allele of
sup-9. To characterize the genetic interactions of nlSS0, we constructed strains with nlSS0 in combination with previously identified mutations in these five genes and also performed mutageneses to identify recessive and dominant suppressors. nlSS0 is completely suppressed by
unc-93(0) and
sup-10(0) mutations and partially suppressed by a
sup-18( 0) mutation. These extragenic suppressors of nlSS0 act semi-dominantly, suggesting a sensitivity to the stoichiometry of these gene products. (Similarly, weak semi-dominant suppression of elS00/+ is seen for sup- 9(0) and
sup-10(0) mutations.) Two of three sup-ll mutations tested act as weak recessive suppressors of nlSS0; the third does not suppress. The identification of a rubber-band allele of
sup-9 provides further evidence that
sup-9 participates in the same process(es) as do
unc-93 and
sup-10. Since
unc-93 encodes a protein that appears to be membrane associated (Levin and Horvitz, CSH C. elegans Mtg. Abst. 1989, p. 151), we propose that these three genes produce protein products that are likely to interact as a complex in the muscle membranes. We have characterized two dominant-negative
sup-9 mutations.
n242 was isolated as a suppressor of elS00 by I. Greenwald and is a semi- dominant suppressor of elS00 and
n983. We isolated
nl435 as a suppressor of
n983.
nl435 is a semi-dominant suppressor of
n983 and a weak recessive suppressor of elSO0. These mutations antagonize
sup-9(+) function based on the semi-dominant nature of the suppression of elS00 and
n983. Both alleles have no visible phenotype alone and map to within 0.2 m.u. of
sup-9. We have shown that
nl435 is a
sup-9 allele by generating cis-dominant
sup-9(0) mutations that inactivate
nl435.