The expression of the hsp16 gene family in Caenorhabditis elegans has been examined by introducing hsp16-lacZ fusions into the nematode by transformation. Transcription of the hsp16-lacZ transgenes was totally heat-shock dependent and resulted in the rapid synthesis of detectable levels of beta-galactosidase. Although the two hsp16 gene pairs of C. elegans are highly similar within both their coding and noncoding sequences, quantitative and qualitative differences in the spatial pattern of expression between gene pairs were observed. The hsp16-48 promoter was shown to direct greater expression of beta-galactosidase in muscle and hypodermis, whereas the hsp16-41 promoter was more efficient in intestine and pharyngeal tissue. Transgenes that eliminated one promoter from a gene pair were expressed at reduced levels, particularly in postembryonic stages, suggesting that the heat shock elements in the intergenic region of an hsp16 gene pair may act cooperatively to achieve high levels of expression of both genes. Although the hsp16 gene pairs are never constitutively expressed, their heat inducibility is developmentally restricted; they are not heat inducible during gametogenesis or early embryogenesis. The hsp16 genes represent the first fully inducible system in C. elegans to be characterized in detail at the molecular level, and the promoters of these genes should find wide applicability in studies of tissue- and developmentally regulated genes in this experimental organism.

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Exposure to microwave radiation enhances the aggregation of bovine serum albumin in vitro in a time-and temperature-dependent manner. Microwave radiation also promotes amyloid ¢bril formation by bovine insulin at 60 ‡C. These alterations in protein conformation are not accompanied by measurable temperature changes, consistent with estimates from ¢eld modelling of the speci¢c absorbed radiation (15^20 mW kg 31 ). Limited denaturation of cellular proteins could explain our previous observation that modest heat-shock responses are induced by microwave exposure in Caenorhabditis elegans. We also show that heat-shock responses both to heat and microwaves are suppressed after RNA interference ablating heat-shock factor function. ß

We report that the free-living nematode Caenorhabditis elegans can respond to a variety of stressors (compounds known to induce the production of cellular stress proteins in model biological systems), by ceasing pharyngeal pumping. This phenomenon results in both a reduction in intake of the stressor and a cessation of feeding. The effect of stressors can therefore be conveniently assayed by monitoring the decrease in the density of the bacterial food in liquid cultures of nematodes. A great range of stressors induced this response including alcohols, heavy metals, sulfhydryl-reactive compounds, salicylate, and heat. For several of these stressors, inhibition of pharyngeal pumping occurred at stressor concentrations below the threshold required for the induction of the 16-kDa heat shock proteins. Salicylate, which did not induce 16-kDa heat shock proteins at any concentration, nevertheless inhibited pharyngeal pumping. Heat was also inhibitory, at a temperature where 16-kDa heat shock protein production was near maximal. Some compounds caused only a partial inhibition of feeding while with others the effect was complete. Upon removal of the stressor, the nematodes resumed pharyngeal pumping with a residual inhibitory effect that depended on the concentration and type of stressor that had been applied. A number of C. elegans neurosensory mutant strains also exhibited a cessation of pharyngeal pumping when exposed to stressors suggesting that the mechanism underlying this inhibition was not entirely neurosensory and may be intrinsic to the pharynx. In C. elegans and other invertebrates, stress-induced inhibition of feeding may be an important survival mechanism that limits the intake of toxic solutes.

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