We have been studying suppressors of the muscle affecting gene
unc-89 which encodes a giant modular polypeptide consisting of Ig and signal transduction domains (please see our abstract at the 1996 C.elegans West Coast Meeting). One such suppressor maps to the left arm of the X chromosome, between
unc-1 and
dpy-3, which is an approx. 3 map unit interval. This suppressor, sup
(sf1), has no phenotype by itself. Previously,
unc-96 was placed in this general region by two-factor mapping. Recently, we have refined the position of
unc-96 by placing it in the same
unc-1 -
dpy-3 interval by three-factor mapping. The only muscle affecting gene in this broad region is
unc-96 (Zengel & Epstein, 1980, Cell Motil. 1, 73-97; Waterston 1988, In: The Nematode C. elegans, pp.281-335). Animals which are mutant for
unc-96(
su151), the only reported allele, are slow moving, reduced to 10-15% of wild type in a motility assay. By polarized light microscopy,
su151 shows increased birefringent "needles" near the ends of muscle cells, without any definite A or I bands. As our suppressor does not have a phenotype, it may be an unusual allele of
unc-96. We are currently trying to determine whether this is the case or not. We have made an
unc-89(
e1460);
unc-96(
su151) double. This animal is not suppressed for the
unc-89 phenotype. In fact, in this double, both Unc-89 and Unc-96 polarized light phenotypes are discernible. We have not complementation tested the suppressor against
su151 because sup
(sf1) acts dominantly. We are using two methods in order to rescue both
unc-96(
su151) and sup
(sf1). First we are using microinjection of YACs. Second, we are crossing our gene into the background of stable transgenic lines which contain cosmids from the
unc-1 -
dpy-3 region, courtesy of the Baillie Lab. We may also have identified a second allele of
unc-96. We were kindly given a strain from Phil Anderson which was originally thought to contain an
unc-89 allele,
r291, isolated as a suppressor of
unc-105. We outcrossed
unc-105 using marked chromosomes. To our surprise
unc-89 was not present. The polarized light phenotype was oddly like
unc-96(
su151) rather than
unc-89. In order to test whether
r291 could be a new allele of
unc-96, we complementation tested it against
su151. The two alleles fail to complement.