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Resources » Paper

Tedesco PM et al. (1991) International C. elegans Meeting "DEFICIENCY MAPPING SHOWS THAT REDUCED HERMAPHRODITE SELF FERTILITY IS SEPARABLE FROM age-1."

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  • Comments on Tedesco PM et al. (1991) International C. elegans Meeting "DEFICIENCY MAPPING SHOWS THAT REDUCED HERMAPHRODITE SELF FERTILITY IS SEPARABLE FROM age-1." (0)

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00020998

    Tedesco PM, Hutchinson T, & Johnson TE (1991). DEFICIENCY MAPPING SHOWS THAT REDUCED HERMAPHRODITE SELF FERTILITY IS SEPARABLE FROM age-1 presented in International C. elegans Meeting. Unpublished information; cite only with author permission.

    We combine classical, quantitative, and molecular genetic analyses in determining whether the age-1 gene, which is involved in the specification of life span, is also involved in the specification of hermaphrodite fertility. In the nematode Caenorhabditis elegans the mutant form of the age-1 gene lengthens life span up to 70% (Age). This gene has been mapped to the center of chromosome 11. The age-1 mutation cosegregates with a temperature-sensitive mutant allele of fer-15 and is also associated with a four-fold reduction in hermaphrodite self fertility (Brd). Deficiencies on chromosome 11 have been used to map these three characters. One class of deficiencies (mnDf92, mnDf94, mnDf98) has a genetic end point to the left of fer-15 and complements fer-15, emb-27, and Brd; a second class of eleven deficiencies (mnDf91, etc.) has a nominal end point to the right of fer-15 and fails to complement fer-15, emb-27, and Brd. Thus, these two classes of deficiencies define a genetic region containing fer-15, emb-27, and the Brd phenotype. Both deficiency classes complement age1 in 11 of 15 possible tests. Complementation mapping with other chromosome 11 deficiencies suggest that age-1 is under mnDf63 and mnDf89, near unc-4. This position agrees with multipoint mapping of Hutchinson et al. fer-15, emb-27, and Brd are also positioned to the physical map by identifying DNA polymorphisms associated with the end points of the first two classes of deficiencies. We have identified the right-hand end point of 10 of 11 deficiencies and the lefthand end point of 5 of 6 deficiencies examined and have mapped the positions of these end points using cosmids from the Rol-6 contig which covers much of chromosome 11. We have also discovered a RFLP that cosegregates with the fer-15(b26ts) mutant allele and presumably results from an alteration other than a single base-pair change. The Brd phenotype in deficiency heterozygotes behaves as a complete recessive at 25 but as an additive or semi-dominant trait at 20 .


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