Owen K. Atkin, John R. Evans and Katharina Siebke
Australian Journal of Plant Physiology 25(4) 437 - 443
Published: 1998
Respiration (
R, non-photorespiratory mitochondrial CO
2release) in leaves is inhibited by light. However, exposure to darkness after a period of illumination can also result in
Rbeing temporarily stimulated (termed ‘light enhanced dark respiration’, LEDR). We used a fast-response CO
2exchange system to investigate these observations in tobacco leaves. After switching off the light, there were two peaks of CO
2release, the first at 15–20 s (the photorespiratory post-illumination burst) and the second at 180–250 s (LEDR). LEDR occurred in all post-illumination experiments, independent of O
2or CO
2concentration. However, LEDR increased with increasing irradiance during the pre-dark period, suggesting some dependency on prior photosynthesis. We investigated the inhibition of
Rby light at low CO
2concentrations (&Ggr;
*): &Ggr;
*is the intercellular CO
2concentration at which net CO
2release represents R in the light. The inhibition of R in the light took about 50 s and was even evident at 3 mmol photons m
-2s
-1, regardless of the light quality (red, blue or white). The inhibition of
Rby light showed similar dependency on irradiance as LEDR, such that the degree of inhibition was positively correlated with the level of LEDR. In the light, switching from 350 ppm to a low CO
2concentration that resulted in the intercellular CO
2concentration being at &Ggr;
*, resulted in
Rinitially increasing and then stabilising. Maintaining the leaf at &Ggr;
*did not, therefore, lead to an underestimation of
R. Our data suggest that a common mechanism may be responsible for both the inhibition of
Rby light and LEDR.
https://doi.org/10.1071/PP97159
© CSIRO 1998
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