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Cell Rep. 2015 Aug 18;12(7):1196-1204. doi: 10.1016/j.celrep.2015.07.026. Epub 2015 Aug 6.

Heterotypic Signals from Neural HSF-1 Separate Thermotolerance from Longevity.

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Howard Hughes Medical Institute, University of California, Berkeley CA 94720, USA.
The Buck Institute for Research on Aging, Novato CA 94945 USA.
Department of Biochemistry, University of Washington, Seattle WA 98195, USA.
Contributed equally


Integrating stress responses across tissues is essential for the survival of multicellular organisms. The metazoan nervous system can sense protein-misfolding stress arising in different subcellular compartments and initiate cytoprotective transcriptional responses in the periphery. Several subcellular compartments possess a homotypic signal whereby the respective compartment relies on a single signaling mechanism to convey information within the affected cell to the same stress-responsive pathway in peripheral tissues. In contrast, we find that the heat shock transcription factor, HSF-1, specifies its mode of transcellular protection via two distinct signaling pathways. Upon thermal stress, neural HSF-1 primes peripheral tissues through the thermosensory neural circuit to mount a heat shock response. Independent of this thermosensory circuit, neural HSF-1 activates the FOXO transcription factor, DAF-16, in the periphery and prolongs lifespan. Thus a single transcription factor can coordinate different stress response pathways to specify its mode of protection against changing environmental conditions.

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