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Resources » Paper

Shawn Ahmed et al. (2002) European Worm Meeting "Does the DNA damage checkpoint shorten lifespan in C. elegans?"

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    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00011407

    Shawn Ahmed, Iuval Clejan, Arno Alpi, & Anton Gartner (2002). Does the DNA damage checkpoint shorten lifespan in C. elegans? presented in European Worm Meeting. Unpublished information; cite only with author permission.

    The DNA damage checkpoint is composed of proteins that sense DNA damage and then send a signal that DNA damage has occurred, which results in either cell cycle arrest and DNA repair (which eliminates the damage) or apoptosis (which eliminates the damaged cell). Recently, we cloned a novel DNA damage checkpoint gene, rad-5/clk-2, which is defined by two alleles, rad- 5(mn159) and clk-2(qm37), which are defective for both the DNA damage checkpoint and the S- phase replication checkpoint (1). One mutant allele of this gene, clk-2(qm37), was previously characterized as one of four clock genes, which, when mutated, display maternal-effect slow growth (Gro), slowed biological rhythms, and an extended lifespan (2). It was suggested that these clock mutants might experience an extended lifespan as a result of slowed metabolic rates (2). Although clk-2(qm37) has a strong maternal-effect slow growth (Gro) phenotype, the rad- 5(mn159) allele is only weakly Gro. However, both rad-5(mn159) and clk-2(qm37) are equally long-lived, suggesting that checkpoint inactivation and not metabolic rate may be the cause of the longevity experienced by these two mutants.


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