Feeding is inhibited by sublethal concentrations of toxicants and by heat stress in the nematode Caenorhabditis elegans: Relationship to the cellular stress response

秀丽隐杆线虫 热休克蛋白 压力源 热冲击 兴奋 生物 线虫 突变体 化学 生物物理学 细胞生物学 生物化学 生态学 解剖 氧化应激 神经科学 基因
作者
D. Jones,E. P. M. Candido
出处
期刊:The journal of experimental zoology [Wiley]
卷期号:284 (2): 147-157 被引量:104
标识
DOI:10.1002/(sici)1097-010x(19990701)284:2<147::aid-jez4>3.3.co;2-q
摘要

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. J. Exp. Zool. 284:147–157, 1999. © 1999 Wiley-Liss, Inc.

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