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Resources » Paper

Driscoll MA et al. (2000) East Coast Worm Meeting "Contributions of WRN-related Helicases to C. elegans Aging"

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    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00010459

    Driscoll MA, Herndon LA, & Nycz KM (2000). Contributions of WRN-related Helicases to C. elegans Aging presented in East Coast Worm Meeting. Unpublished information; cite only with author permission.

    Four genes in the C. elegans genome exhibit sequence similarity to the RecQ family of DNA helicases which include the human Werner (WRN), Bloom (BLM) and Rothmund-Thomson (RTS) syndrome genes. Mutation of human WRN and RTS can confer features of accelerated aging. Both WRN and RTS patients have a high rate of genome instability, which is also a key feature of patients with Bloom syndrome. Similarly, mutation of the yeast RecQ homolog, SGS1, results in a high rate of genomic instability and a lifespan 40% shorter than wild type1, 2. To determine if the RecQ family of helicases share similar functions in C. elegans, we generated deletions within the C. elegans gene most closely related to the Werners gene (F18C5.2) and in another homolog (E03A3.2) and have tested these strains for lifespan and genomic instability. Preliminary results indicate that animals lacking F18C5.2 or E03A3.2 are viable and fertile. They have normal lifespans and do not have a high rate of genomic instability. Since C. elegans has four related helicases, there may be redundancy in the activity of these helicases. To test this hypothesis, we are now analyzing animals that carry mutations in multiple DNA helicase family members. It has recently been determined that him-6 mutant animals, which have a high rate of chromosome nondisjunction, contain mutations in the C. elegans DNA helicase gene T04A11.6, which is most closely related to the human BLM gene3. We are also testing mutants for UV radiation or X-ray hypersensitivity, since it is possible that these helicases play a role in DNA repair. We are testing the expression pattern of these genes and are screening for a deletion in the fourth remaining C. elegans DNA helicase family member, K02F3.1. By establishing a nematode model for accelerated aging disorders, we hope to extend understanding of the action of helicase family members in senescence and learn more about mechanisms of aging overall. Watt, P.M., I.D. Hickson, R.H. Borts and E.J. Louis. 1996. Genetics 144: 935. Sinclair, D.A., K. Mills and L. Guarente. 1997. Science 277: 1313. Wicky, C., A. Rose and F. Mueller. 1998. European Worm Meeting Abstract.


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