Research ArticleCell Biology

Olfactory experience primes the heat shock transcription factor HSF-1 to enhance the expression of molecular chaperones in C. elegans

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Science Signaling  17 Oct 2017:
Vol. 10, Issue 501, eaan4893
DOI: 10.1126/scisignal.aan4893

Learning the smell of danger

The best way to prevent pathogen-induced cellular damage is to avoid becoming infected. If that is not possible, being prepared to fight damage is the next-best option. Ooi and Prahlad found that previous experience of the odor of a pathogenic bacterium enhanced the pathogen avoidance response of the nematode Caenorhabditis elegans. In addition, this experience enhanced heat shock factor 1 (HSF-1) target gene expression when animals encountered the pathogen, thus increasing survival. Olfactory experience of the pathogen odor alone caused HSF-1 to accumulate at genomic loci enriched for RNA polymerase II. These responses required serotonergic signaling, which is important for learning and memory. The activation of HSF-1 and chaperone expression has been considered an autonomous reaction of cells to protein damage. Instead, the authors show that in C. elegans, olfactory learning can initiate HSF-1–dependent chaperone gene expression systemically in anticipation of a proteotoxic encounter.

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