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Resources » Paper

Morris JZ et al. (1996) East Coast Worm Meeting "THE C. elegans PHOSPHATIDYLINOSITOL 3-KlNASE HOMOLOGUE AGE-1 REGULATES DAUER ARREST AND SENESCENCE"

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  • Comments on Morris JZ et al. (1996) East Coast Worm Meeting "THE C. elegans PHOSPHATIDYLINOSITOL 3-KlNASE HOMOLOGUE AGE-1 REGULATES DAUER ARREST AND SENESCENCE" (0)

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00010900

    Morris JZ, Tissenbaum HA, & Ruvkun GB (1996). THE C. elegans PHOSPHATIDYLINOSITOL 3-KlNASE HOMOLOGUE AGE-1 REGULATES DAUER ARREST AND SENESCENCE presented in East Coast Worm Meeting. Unpublished information; cite only with author permission.

    A pheromone-induced neurosecretory signaling system in C. elegans triggers an arrest of development and of senescence at the dauer stage. age-1 is a key gene in this neuroendocrine pathway whose activity is required for both nonarrested development and normal senescence. We present evidence that age-1 is the same gene as daf-23 and that ag-1 encodes a member of the family of phosphatidylinositol 3-kinase (PI 3-kinase) catalytic subunits. Four age-1 mutant alleles affect this PI 3-kinase homologue: two lesions are stop codons that truncate the protein at distinct locations N terminal to the kinase domain and thus are likely to define the age-l null phenotype. Maternal age-1 activity is specifically abrogated in one age-1 mutant which was isolated on the basis of its enhanced longevity. Lack of either maternal or zygotic age-1 gene activity confers long life span but not developmental arrest whereas lack of both maternal and zygotic activity causes arrest at the dauer stage. These data suggest that decreased AGE-1-mediated phosphatidylinositol(3,4,5)P3(PIP3) signaling leads to increased longevity, whereas complete lack of this signaling leads to developmental arrest.

    Affiliation:
    - Department of Molecular Biology Massachusetts General Hospital Boston, MA 02114 Department of Genetics, Harvard Medical School


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