A screen for nonconditional dauer-constitutive mutations in Caenorhabditis elegans.

Authors: Malone EA; Thomas JH

Abstract: In Caenorhabditis elegans, formation of the developmentally arrested dauer larva is induced by high levels of a constitutively secreted pheromone. Synergy between two groups of incompletely penetrant dauer-constitutive (Daf-c) mutations has recently led to a proposal that these two groups of genes are partially redundant and function in two parallel pathways that regulate dauer formation. A possible weakness in this reasoning is that the mutations used to identify the synergy were specifically obtained as incompletely penetrant mutations. Here we use screens to identify new Daf-c alleles without any requirement for partial penetrance. Nevertheless, 22 of the 25 new mutations are incompletely penetrant mutations in 6 previously identified genes. Among these are mutations in daf-8 and daf-19, genes for which only one mutation had been previously identified. Also included in this group are three daf-1 alleles that do not exhibit the maternal rescue characteristic of other daf-1 alleles. Two of the 25 new mutations are fully penetrant and are alleles of daf-2, the one gene in which a fully penetrant mutation had been found earlier. Finally, one of the 25 new mutations is semidominant, temperature-sensitive, and identifies a new gene, daf-28. The results demonstrate that an incompletely penetrant Daf-c phenotype is characteristic of mutations in most Daf-c genes other than daf-2. This finding strengthens the hypothesis that a branched genetic pathway controls dauer formation.

Keywords: Alleles; Animals; Caenorhabditis elegans/*genetics/growth & development/physiology; Genes, Helminth; Larva/genetics/growth & development; Models, Genetic; Mutagenesis; Mutation; Phenotype; Pheromones/secretion; Temperature
Journal: Genetics
Volume: 136
Issue: 3
Pages: 879-86
Date: March 1, 1994
PMID: 8005442
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Malone EA, Thomas JH (1994) A screen for nonconditional dauer-constitutive mutations in Caenorhabditis elegans. Genetics 136: 879-86.

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