Earlier studies have shown
unc-2 to be a putative alpha-1 calcium channel subunit affecting a variety of behaviors and expressed in many different neurons. We have shown previously isolated
unc-2 alleles to be hypersensitive to serotonin, unable to adapt to dopamine, and Egl-c, in addition to exhibiting a slow-moving uncoordinated phenotype. However, known
unc-2 mutants are viable, fertile, and mate well. Of the known alleles of
unc-2 only one has been sequenced (
unc-2(
mu74)), which is a deletion removing most of domain IV, but it is not known whether this or any other existing allele exhibits the null phenotype. We are attempting to isolate new deletion alleles of
unc-2 using an
unc-2(
pk95) strain received from Ron Plasterk that contains a Tc1 insertion in a large intron of the
unc-2 gene, an active mutator element causing active transposition, and a linked dumpy mutation allowing us to follow the
pk95 chromosome in crosses. To screen for these alleles we took
unc-2(
pk95) hermaphrodites and mated them to
unc-2(
mu74) males and looked for non-Dpy Unc's in the F1 generation resulting from a failure to complement the
unc-2(
mu74) mutation. So far, one allele has been isolated, a more extensive deletion than
mu74 although still viable and fertile, that removes much of domain III and part of domain IV and the III-IV cytoplasmic domain. Progress in isolating more deletion alleles will be discussed later. These new alleles will also allow us to determine the specificity of antibodies generated to the UNC-2 protein.