Carbon dioxide-induced bioluminescence increase in Arachnocampa larvae.

ABSTRACT

Arachnocampa larvae utilise bioluminescence to lure small arthropod prey into their web-like silk snares. The luciferin-luciferase light-producing reaction occurs in a specialised light organ composed of Malpighian tubule cells in association with a tracheal mass. The accepted model for bioluminescence regulation is that light is actively repressed during the non-glowing period and released when glowing through the night. The model is based upon foregoing observations that carbon dioxide (CO2) - a commonly used insect anaesthetic - produces elevated light output in whole, live larvae as well as isolated light organs. Alternative anaesthetics were reported to have a similar light-releasing effect. We set out to test this model in Arachnocampa flava larvae by exposing them to a range of anaesthetics and gas mixtures. The anaesthetics isoflurane, ethyl acetate and diethyl ether did not produce high bioluminescence responses in the same way as CO2 Ligation and dissection experiments localised the CO2 response to the light organ rather than it being a response to general anaesthesia. Exposure to hypoxia through the introduction of nitrogen gas combined with CO2 exposures highlighted that continuity between the longitudinal tracheal trunks and the light organ tracheal mass is necessary for recovery of the CO2-induced light response. The physiological basis of the CO2-induced bioluminescence increase remains unresolved, but is most likely related to access of oxygen to the photocytes. The results suggest that the repression model for bioluminescence control can be rejected. An alternative is proposed based on neural upregulation modulating bioluminescence intensity.