Worm Breeder's Gazette 14(5): 44 (February 1, 1997)

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

New Alleles of unc-96?

Tina Tinley1, Christine Alberico1, David Baillie2, Guy Benian1

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

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
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.