The mutation pl 156 is an anomalous allele of the cha-l complex locus - it fails to complement both
cha-1 and
unc-17 mutations (Rand and Russell, 1984). A screen for suppressors of the Unc phenotype associated with
p1156 homozygotes produced 10 independent suppressors. For each of them, suppression was recessive, and suppressor homozygotes had a Smg phenotype. Mapping and complementation analysis indicated that 9 suppressors were alleles of
smg-1 and the tenth was an allele of
smg-5. Phenotypic analysis with reference alleles of all 6 smg genes indicates that mutations in any of the smg genes completely (and recessively) suppress the slow growth and small size phenotypes of
p1156 homozygotes. Suppression of the Unc phenotype is strong but not total. pl
l56 homozygotes are also strongly resistant to inhibitors of acetylcholinesterase; this resistance is completely suppressed by
smg-2,
smg-3,
smg-4, or
smg-5, but only partially suppressed by smg-l or
smg-6. Animals homozygous for
p1156 are also deficient for choline acetyltransferase (ChAT) activity; this phenotype is not suppressed by smg mutations. Thus, the phenotypic suppression by smg mutations is not due to restoration of ChAT activity. We have determined that
p1156 represents an ~730 bp deletion in the middle of the
cha-1 complex. The location of the deletion suggests that it disrupts both the cha-l and the putative
unc-17 transcripts ( see abstract by Rand, et al.); thus pl
l56 may effectively represent a cha-l
unc-17 double mutant. We tentatively conclude that the cha-l defect in pl 156 is relatively mild and the
unc-17 defect is relatively severe; presumably, it is the
unc-17 defect which is suppressed by smg mutations. Supported by grants from MDA and the Oklahoma Center for the Advancement of Science and Technology.