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FIREFLY FLASHING IS CONTROLLED BY GATING OXYGEN TO LIGHT-EMITTING CELLS

GRAHAM S. TIMMINS1,*, FRASER J. ROBB2,{ddagger}, CARMEN M. WILMOT2, SIMON K. JACKSON1 and HAROLD M. SWARTZ2

1 Department of Medical Microbiology, University of Wales College of Medicine, Cardiff, UK
2 Department of Radiology, Dartmouth Medical School, Hanover NH 03755, USA
* Author for correspondence (e-mail: mail{at}eprimaging.com ) at present address: College of Pharmacy, 2502 Marble NE, Albuquerque, NM 87131-5691, USA
{ddagger} Present address: USA Instruments Inc., Aurora, OH 44202, USA



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Fig. 1. Temporal sequence of events in a typical single firefly flash (adapted from data in Buck et al., 1963Go).

 


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Fig. 2. Diagrams (adapted from Ghiradella, 1977Go; Ghiradella, 1998Go, with permission) depicting changes in tracheolar fluid length responsible for controlling oxygen access to the photocytes. (A) Increased fluid length during no light emission; (B) decreased fluid length during light emission. P, photocytes; NE, nerve ending; t, tracheole; TF, tracheolar fluid; T, trachea; TC, tracheolar cell; TEC, tracheal end cell. As explained more fully in the text and shown in Movie 4, neural stimulation leads to a transient increase in the osmotic potential of the tracheolar cell, resulting in decreased tracheolar fluid levels. The resultant decreased diffusional barrier allows greater oxygen supply to the photocytes, relieving intracellular anoxia and enabling light emission (molecular oxygen is required). As tracheolar cell osmotic potential returns to the resting state, tracheolar fluid levels increase, oxygen diffusion to the photocytes is decreased, intracellular anoxia occurs in the photocytes and light emission is inhibited.

 





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