{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T15:17:00Z","timestamp":1783351020003,"version":"3.54.6"},"reference-count":40,"publisher":"National Academy of Sciences","issue":"10","license":[{"start":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T00:00:00Z","timestamp":1772582400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000925","name":"DHAC | National Health and Medical Research Council","doi-asserted-by":"publisher","award":["GNT1137645"],"award-info":[{"award-number":["GNT1137645"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"DHAC | National Health and Medical Research Council","doi-asserted-by":"publisher","award":["GNT2000766"],"award-info":[{"award-number":["GNT2000766"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2026,3,10]]},"abstract":"<jats:p>\n                    The mitochondrial unfolded protein response (UPR\n                    <jats:sup>mt<\/jats:sup>\n                    ) is triggered by cells to alleviate proteotoxicity in response to metabolic stress. The ability to anticipate and prime cells against mitochondrial stress, by sensing potentially toxic changes in the external or internal environment, would provide a survival advantage. Yet, whether and how animals anticipate mitochondrial stress remains unclear. Here, we show that the\n                    <jats:italic toggle=\"yes\">\n                      <jats:italic toggle=\"yes\">Caenorhabditis elegans<\/jats:italic>\n                    <\/jats:italic>\n                    receptor guanylyl cyclase GCY-9 regulates neuropeptide signaling from carbon dioxide\u2013sensing neurons to govern a noncanonical mitochondrial stress response in the intestine. This noncell autonomous stress response induces atypical mitochondrial chaperone transcription, confers mitochondrial stress resistance, and increases mitochondrial membrane potential and respiration. We show that starvation decreases GCY-9 expression and propose that the resultant cytoprotective program is launched to offset metabolic and proteotoxic risks. Thus, environmental sensing by peripheral neurons can preemptively enhance systemic mitochondrial function in response to metabolic uncertainty.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2525619123","type":"journal-article","created":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T18:40:32Z","timestamp":1772649632000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":2,"title":["Gas-sensing neurons prime mitochondrial fitness to offset metabolic stress"],"prefix":"10.1073","volume":"123","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7242-1283","authenticated-orcid":false,"given":"Rebecca","family":"Cornell","sequence":"first","affiliation":[{"name":"Development and Stem Cells Program, Monash Biomedicine Discovery Institute, Monash University","place":["Melbourne, Australia"]},{"name":"Department of Anatomy and Developmental Biology, Monash University","place":["Melbourne, 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