Adverse effects of metal exposure on chemotaxis towards water-solubleattractants regulated mainly by ASE sensory neuronin nematode Caenorhabditis elegans

Chemotaxis to water-soluble attractants is mainly controlled by ASE sensory neuron whose specification is regulated by che-1 inCaenorhabditis elegans. Our data suggested that exposure to high concentrations of metals, such as Pb, Cu, Ag, and Cr, would resultin severe defects of chemotaxis to water-soluble attractants of NaCl, cAMP, and biotin. Moreover, the morphology of ASE neuronstructures as observed by relative fluorescent intensities and relative size of fluorescent puncta of cell bodies, relative lengths of sensoryendings in ASE neurons, and the expression patterns of che-1 were obviously altered in metal exposed animals when they meanwhileexhibited obvious chemotaxis defects to water-soluble attractants. In addition, the dendrite morphology could be noticeably changedin animals exposed to 150 mol/L of Pb, Cu, and Ag. Furthermore, we observed significant decreases of chemotaxis to water-solubleattractants in Pb exposed che-1 mutant at concentrations more than 2.5 mol/L, and in Cu, Ag, and Cr exposed che-1 mutant atconcentrations more than 50 mol/L. Therefore, impairment of the ASE neuron structures and functions may largely contribute to theappearance of chemotaxis defects to water-soluble attractants in metal exposed nematodes.