Certain mutations in the
unc-105 II gene of the nematode Caenorhabditis elegans have dominant effects on morphology and behavior: animals become small, severely hypercontracted and paralyzed. These
unc-105 mutants revert both spontaneously and with mutagens at high frequencies to a wild-type phenotype. Most of the reversion events are intragenic, apparently because the null (loss-of- function) phenotype of
unc-105 is wild type. One revertant defined an extragenic suppressor locus,
sup-20 X. Such suppressor alleles of sup- 20 are rare, and the apparent null phenotype of
sup-20 is embryonic lethality. By constructing animals genetically mosaic for
sup-20, we have shown that the primary effect of
sup-20 is in muscle cells. In addition to mutations in
sup-20, other mutations causing muscle defects, such as
unc-54 and
unc-22 mutations, suppress the hypercontracted phenotype of
unc-105. The ease of identifying nonhypercontracted revertants of
unc-105 mutants greatly facilitates the isolation of new mutants defective in muscle structure and function.