C. elegans unc-105 mutations affect muscle and are suppressed by other mutations that affect muscle.
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.[1]References
- C. elegans unc-105 mutations affect muscle and are suppressed by other mutations that affect muscle. Park, E.C., Horvitz, H.R. Genetics (1986) [Pubmed]
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