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Resources » Paper

Christina Dittrich et al. (2006) European Worm Meeting "Identifying Novel Genes Involved in DNA Damage Response Pathways in C. elegans"

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    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00027571

    Christina Dittrich, & Michael O. Hengartner (2006). Identifying Novel Genes Involved in DNA Damage Response Pathways in C. elegans presented in European Worm Meeting. Unpublished information; cite only with author permission.

    Christina Dittrich and Michael O. Hengartner1. Upon DNA damage, a cell responds by arresting its cell cycle, changing its transcription patterns, recruiting the repair machinery or, most severely, by executing its own death by apoptosis. Malfunction of any of these pathways allows cells to replicate in spite of DNA lesions, and thus their genomes accumulate mutations and becomes unstable, a hallmark of tumor cells. Therefore, it is not only of paramount biological, but also of high medical interest, to understand the molecular pathways underlying DNA damage responses. Genotoxic stress induces in the germ line of Caenorhabditis elegans a spectrum of DNA damage responses similar to that observed in humans. Because important genes are often conserved throughout evolution, studies in C. elegans might improve our understanding of the molecular programmes safeguarding the genome of human cells. Wild-type C. elegans animals carry out proper DNA damage responses following exposure to ionizing radiation (IR), thus most of their progeny survive. In contrast, radiation-sensitive (Rad) mutants, which are defective in these pathways, show high levels of embryonic lethality upon IR. Taking advantage of this phenotype, we performed a forward genetic screen and identified 17 mutants whose embryos show reduced viability following IR treatment. Two of those mutants, op442 and op444, display a strong Rad phenotype. We are currently mapping the affected genes taking advantage of molecular polymorphisms between the Bristol and the Hawaii isolate of C. elegans. Additionally, we are characterising those two mutants further in order to learn more about the molecular nature underlying the observed defects.


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