APRILLE*, J.R.*; LAGACE, C.J.; LEWIS, S.M.; MICHEL, T.; MODICA-NAPOLITANO, J.S.; TRIMMER B.A. AND ZAYAS, R.M.; Univ. of Richmond, Richmond VA; Tufts Univ. School of Medicine, Boston, MA; Tufts Univ., Medford MA; Harvard Med School, Boston MA ; Merrimack College, North Andover MA; Tufts Univ., Medford MA: Role of Nitric Oxide and Mitochondria in Control of Firefly Flash

In a recent report (Science 292:2486-88, 2001)we showed that:(1) nitric oxide gas (NO) stimulates light production in Photuris sp in the presence of oxygen; (2) NO scavengers block bioluminescence induced by the neurotransmitter octopamine; and (3) NO synthase is present in lantern cells. These findings suggested key roles for NO and oxygen in the mechanism of flash control. We proposed that NO, produced in response to nerve signals, inhibits respiration in photocyte mitochondria. Mitochondria are clustered in the cell periphery, so active respiration would make the interior regions relatively hypoxic. Inhibition of mitochondrial oxygen consumption would allow available oxygen to pass through to the centrally-located peroxisomes where the oxygen-triggered light reaction is sequestered. New data show that NO does inhibit respiration in isolated lantern mitochondria prepared by differential centrifugation. A standard polarographic assay was used to measure oxygen consumption. When an NO donor drug (NOC-7, 4 �M) was introduced, respiration was completely inhibited. Inhibition was reversed by bright light, and was reinstated when the light was turned off. The results support the idea that NO triggers light production by reversible inhibition of mitochondrial respiration. The data also suggest that the light produced could relieve NO inhibition thus contributing to rapid on/off switching.