Homeostatic control of stearoyl desaturase expression via patched-like receptor PTR-23 ensures the survival of C. elegans during heat stress.

Organismal responses to temperature fluctuations include an evolutionarily conserved cytosolic chaperone machinery as well as adaptive alterations in lipid constituents of cellular membranes. Using C. elegans as a model system, we asked whether adaptable lipid homeostasis is required for survival during physiologically relevant heat stress. By systematic analyses of lipid composition in worms during and before heat stress, we found that unsaturated fatty acids are reduced in heat-stressed animals. This is accompanied by the transcriptional downregulation of fatty acid desaturase enzymes encoded by fat-1, fat-3, fat-4, fat-5, fat-6, and fat-7 genes. Conversely, overexpression of the Δ9 desaturase FAT-7, responsible for the synthesis of PUFA precursor oleic acid, and supplementation of oleic acid causes accelerated death of worms during heat stress. Interestingly, heat stress causes permeability defects in the worm's cuticle. We show that fat-7 expression is reduced in the permeability defective collagen (PDC) mutant, dpy-10, known to have enhanced heat stress resistance (HSR). Further, we show that the HSR of dpy-10 animals is dependent on the upregulation of PTR-23, a patched-like receptor in the epidermis, and that PTR-23 downregulates the expression of fat-7. Consequently, abrogation of ptr-23 in wild type animals affects its survival during heat stress. This study provides evidence for the negative regulation of fatty acid desaturase expression in the soma of C. elegans via the non-canonical role of a patched receptor signaling component. Taken together, this constitutes a skin-gut axis for the regulation of lipid desaturation to promote the survival of worms during heat stress.

Amphid sensory neurons of Caenorhabditis elegans orchestrate its survival from infection with broad classes of pathogens.

The survival of a host during infection relies on its ability to rapidly sense the invading pathogen and mount an appropriate response. The bacterivorous nematode Caenorhabditis elegans lacks most of the traditional pattern recognition mechanisms. In this study, we hypothesized that the 12 pairs of amphid sensory neurons in the heads of worms provide sensing capability and thus affect survival during infection. We tested animals lacking amphid neurons to three major classes of pathogens, namely-a Gram-negative bacterium Pseudomonas aeruginosa, a Gram-positive bacterium Enterococcus faecalis, and a pathogenic yeast Cryptococcus neoformans By using individual neuronal ablation lines or mutants lacking specific neurons, we demonstrate that some neurons broadly suppress the survival of the host and colonization of all pathogens, whereas other amphid neurons differentially regulate host survival during infection. We also show that the roles of some of these neurons are pathogen-specific, as seen with the AWB odor sensory neurons that promote survival only during infections with P aeruginosa Overall, our study reveals broad and specific roles for amphid neurons during infections.