Genetic studies of mei-1 gene activity during the transition from meiosis to mitosis in Caenorhabditis elegans

Article Abstract:

An alternate genetic screen for dominant ct46 defect suppressors defined a new type of intragenic suppressors of mei-1 that appears at high frequency. Analysis of the properties of these alleles in trans-heterozygous combination with known mei-1 alleles resulted in the identification of the mei-1 gene product's role during embryogenesis and suggested the existence of a threshold for mei-1 activity, where a certain amount is necessary for meiosis but must be removed before the onset of mitosis. Results also revealed that trans-suppressors behave antimorphically to reduce mei-1 activity during meiosis and mitosis.

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Mutations in the unc-52 gene responsible for body wall muscle defects in adult Caenorhabditis elegans are located in alternatively spliced exons

Article Abstract:

Genetic experiments indicate that mutations of the unc-52 gene in Caenorhabditis elegans leads to body wall muscle defects. Lethal terminal phenotype is generated by the St549 and ut111 alleles of unc-52, while five other mutations result in paralyzed animals. Sequential analysis enables the determination of sequence alterations generating these mutant phenotypes. Five mutations responsible for the paralysis are located in three adjacent, alternatively spliced exons. Most of these animals have a G to A sequence alteration in an upstream splice acceptor site and the original class 1 mutations.

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Mutations in the sup-38 gene of Caenorhabditis elegans suppress muscle-attachment defects in unc-52 mutants

Article Abstract:

Intergenic suppressors of the unc-52 class 1 mutants of the nematode Caenorhabditis elegans were isolated and characterized. These suppressors are also mutations of the alleles of the sup-38 gene. These suppressors exhibit gonad and muscle derangements on their own. However, when suppressors are present together with the class 1 mutantation of unc-52, muscle derangements are suppressed but gonadal abnormalities are not corrected. Mutations in the sup-38 gene cannot correct abnormalities due to other classes of unc-52 mutation.

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