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Resources » Paper

VanDuyn, Natalia et al. (2009) International Worm Meeting "Molecular and genetic analysis in a novel model of methylmercury neurotoxicity."

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  • Comments on VanDuyn, Natalia et al. (2009) International Worm Meeting "Molecular and genetic analysis in a novel model of methylmercury neurotoxicity." (0)

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    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00033981

    VanDuyn, Natalia, Settivari, Raja, Asikainen, Suvi, Rudgalvyte, Martina, Wong, Garry, & Nass, Richard (2009). Molecular and genetic analysis in a novel model of methylmercury neurotoxicity presented in International Worm Meeting. Unpublished information; cite only with author permission.

    Methylmercury (MeHg) exposure from occupational, environmental and food sources is a significant threat to public health. The toxicant easily passes the blood brain barrier and can cause severe psychological and neurological problems. Although MeHg poisonings have been studied for decades, the molecular determinants involved in the cellular pathology are largely unknown. We have developed a novel model of methylmercury toxicity in the genetically tractable nematode C. elegans. We show that MeHg exposure confers animal death at low toxicant concentrations, and that the sensitivity is partially dependent on growth medium. Consistent with vertebrate studies, growth in the presence of selenium dramatically rescues the MeHg-induced death, and this effect is dependent on a live bacteria food source. Developmental defects are also observed as older larvae exposed to non-lethal doses of MeHg produce progeny that arrest as embryos in utero. Furthermore, exposure of younger larvae to similar concentrations of MeHg results in over a 2-fold delay in development. MeHg-induced reductions in pharyngeal pumping and egg-laying suggest toxicant-induced changes in neuronal signaling. Whole genome microarray and real-time PCR results show a strong induction of specific heat shock proteins and glutathione-S-transferases following exposure to MeHg. Gene expression studies also indicate a significant induction of genes involved in electron transport, cell growth and protein folding. MeHg also differentially affects the regulation of a miRNA targeting a serpentine receptor as well as other genes involved in growth and neurodevelopment, and further support possible toxicant-induced dysfunction in neurotransmitter signaling. Overall these studies suggest that C. elegans is a powerful model system to explore the molecular basis of MeHg toxicity. Support Contributed By: NIH R011ES014459 and Vanderbilt University Toxicology Program Grant (RN).


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