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

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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.
Oxford University Press (OUP)
Title: A screen for nonconditional dauer-constitutive mutations in Caenorhabditis elegans.
Description:
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.

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