Torres López, MaríaSpiller, Pedro FGao Chen, LinGarcía-Flores, PaulaMurphy, Michael POrtega Sáenz, PatriciaLópez Barneo, José2025-06-102025-06-102025-02-21Torres López, M., Spiller, P.F., Gao Chen, L., García-Flores, P., Murphy, M.P., Ortega Sáenz, P. y López Barneo, J. (2025). Acute oxygen sensing by arterial chemoreceptors with a mutant mitochondrial complex I ND6 subunit lacking reverse electron transport. FEBS letters, 599 (8), 1122-1134. https://doi.org/10.1002/1873-3468.70017.0014-57931873-3468https://hdl.handle.net/11441/174169Carotid body glomus cells are essential for stimulating breathing in response to hypoxia. They contain specialized mitochondria in which hypoxia induces the accumulation of NADH and H 2O 2 that modulate membrane ion channel activity. We investigated whether hypoxia induces reverse electron transport (RET) at mitochondrial complex I (MCI). We studied glomus cells from mice with a mutation in ND6, a core protein of MCI, which maintain normal MCI NADH dehydrogenase activity but cannot catalyze RET. The ND6 mutation increases the propensity of MCI to deactivate, and glomus cells with deactivated MCI are insensitive to acute hypoxia. These findings further indicate that MCI function is necessary for glomus cell responsiveness to hyp- oxia, although MCI RET does not seem to be required for this process.application/pdf13 p.engAcute oxygen sensingCarotid body glomus cellsHypoxiaMitochondrial complex I deactivationND6 mutationReverse electron Transportinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccesshttps://doi.org/10.1002/1873-3468.70017