sup-5 is a member of a group of interacting genes (
unc-93,
sup-9,
sup-10,
sup-11, and
sup-18) involved in muscle structure and function.
unc-93(
e1500), 00), and
sup-10(
n983) are rare, altered-function mutations that confer a distinctive uncoordinated ( 'rubberband'), muscle-defective phenotype. When a rubberband mutant is prodded on its head, the worm contracts and then relaxes without moving backwards, while a wild-type worm simply moves backwards. This rubberband phenotype suggests that the worm can contract its muscles but that the regulation or coordination of the contraction is defective. Null alleles of
unc-93,
sup-10, and
sup-18 result in a wild-type phenotype alone and are recessive suppressors of
e1500 and
n983. The wild-type null phenotype of four of these five genes suggests they may be functionally redundant. Certain rare alleles of
sup-11 (including
n403) act as dominant suppressors of
unc-93(
e1500) and recessive suppressors of
sup-10(
n983); the
sup-11 null phenotype is embryonic lethality. Our model for the interaction of these genes is that the rubberband mutations produce abnormal gene products that disrupt a redundant process in the regulation of muscle contraction, but the absence of the gene products of four of these genes does not adversely affect muscle contraction. A new rubberband mutation,
n1550, was isolated by M. Herman in an unrelated screen.
n1550 is the strongest rubberband mutation identified. It has a dominant uncoordinated phenotype and a recessive phenotype of extreme sluggishness, very slow growth, and the production of few, if any, progeny. We have assigned
n1550 as an allele of
sup-9 based on two observations. First,
n1550 maps to the same region of chromosome II as does
sup-9 (by two-factor data with
lin-31 II and being uncovered by nDf3). Second, an F1 reversion screen of
n1550 yields
sup-9 null alleles. (We screened for wild-type F1 progeny from EMS-mutagenized
sup-9(
n1550); 500
n1415)
dpy-17(
e164) hermaphrodites mated with
lin-42(
n1089)/+ males.) Because reversion of the Unc phenotype associated with
n1550 results in cis-dominant
sup-9 null mutations and
sup-9 null mutations do not suppress
n1550 in trans, this experiment indicates that
n1550 is an allele of
sup-9.The pattern of suppression for
sup-9(
n1550) is as follows: (1)
n1550 is completely suppressed by an
unc-93(0) mutation. (2)
n1550 is completely suppressed by a
sup-10(0) mutation. (3)
n1550 is partially suppressed by a
sup-18(0) mutation. (4)
n1550 is not suppressed by
sup-11(
n403). This suppression pattern differs from that for the other rubberband alleles because
n1550 is not suppressed by
sup-11(
n403).
n1550, like
unc-93(
e1500), is only partially suppressed by
sup-18; by contrast, a weaker rubberband allele,
sup-10(
n983), is fully suppressed by
sup-18. All the extragenic suppressors of
n1550 act semi-dominantly, suggesting a stoichiometry among these gene products . The identification of a rubberband 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, J. Z. and Horvitz, B., CSH C. elegans Meeting Abstracts 1989,
p151), we propose that these three genes produce gene products that are likely to interact as a protein complex in the muscle membranes.