Entomopathogenic nematodes are one of the most important biological control agents for insect pests. One major obstacle in using entomopathogenic nematodes is lack of storage stability compared to chemical pesticides. Entomopathogenic nematodes under environmental stress (i.e., desiccation) develop into a infective juvenile stage analogous (phylogenetically similar) to the dauer stage in the free-living nematode Caenorhabditis elegans. The genetic pathway in dauer juvenile formation has been extensively studied in C. elegans. However, few studies on the biochemical and physiological changes that occur when C. elegan dauer juveniles are exposed to extreme environmental conditions have been conducted. Therefore, we sought to study the genetic expression of stress genes in C. elegans as they relate to desiccation tolerance in entomopathogenic nematodes.
We have cloned five stress genes [glycogen synthase (Sf gsy-1) from Steinernema feltiae IS-6 (Zitman-Gal et al., 2000), trehalose phosphate-6-synthase (Ce tsp-1) from Caenorhabditis elegans (Brey et al., unpublished data), trehalose phosphate-6-synthase (Sc tsp-1) from Saccharomyces cerevisiae and hemolymph desiccation stress protein gene (Tm dsp28) from Tenebrio molitor (provided by V.K. Walker] into expression vectors. We have shown that overexpression of one of the genes, trehalose-6-phosphate synthase gene (tsp-1Ce), increases desiccation tolerance in transformed C. elegans compared to non-transformed C. elegans. Currently, we are in the process of transforming C. elegans with the other four stress genes. We will present and discuss our physiological and molecular results of the five genes at the meeting.
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