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.

Affiliation:
- Department of Pathology, Emory University, Atlanta, GA, 30322 Department of Biological Sciences, Simon Fraser University, Burnaby, British Columbia, CANADA, V5A 1S6