Abstract
Nematode infections compromise human health and reduce agricultural productivity. Experiments that exploit the powerful molecular genetics of the free-living nematodeCaenorhabditis elegans have contributed to our understanding of how the major classes of anthelmintic nematocides kill worms and how worms might evolve resistance to these drugs. InC. elegans, as in parasites, benzimidizoles interfere with microtubule polymerization, the imidazothiazoles/tetrahydropyrimidines activate nicotinic acetylcholine receptors, and the macrocyclic lactones activate glutamate-gated chloride channels. Mutant alleles of genes that encode drug targets often confer resistance inC. elegans. Preliminary evidence suggests that alleles of homologous genes in parasites will, in many cases, also play a role in resistance. Thus, information acquired fromC. elegans can be usefully applied to understand the mechanisms of drug sensitivity and the genetics of resistance in parasites.
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