DISENTANGLING THE ORIGIN OF THE KOK EFFECT USING POSITION SPECIFIC GLUCOSE LABELING IN SUNFLOWER LEAVES

Abstract:

In plants, leaf mitochondrial respiratory CO₂ release is inhibited by light. Bessel Kok first demonstrated this inhibition in 1948. Based on curves of CO₂ assimilation vs irradiance, it is understood that respiration is maximal in the dark. It then frequently decreases linearly with irradiance until reaching some value around the compensation point, beyond which it is constant. CO₂ released by mitochondrial respiration is the result of decarboxylation through pyruvate dehydrogenase (PDH), the tricarboxylic acid pathway (TCAP) and the oxydative pentose phosphate pathway (OPPP). The overall activity of these three reactions is reduced by light. However, their individual contributions to the Kok effect are unknown. We measured the rate of decarboxylation of glucose, position-specifically labeled with ¹³C, to evaluate the participation of PDH, TCAP and OPPP in the Kok effect of sunflower. Leaves were fed with labeled glucose through their transpiration stream. The δ¹³C of the CO₂ released by the leaf was then measured as a function of irradiance. The results showed that the inhibition of the decarboxylation of carbon positions 3 and 4 in glucose is at the origin of the Kok effect. These are the positions of carbon atoms decarboxylated by PDH. In addition, the rate of decarboxylation of position 1 was not different in the light and in the dark. Thus OPPP plays no role in the Kok effect in sunflower leaves. This work improves our current understanding of leaf mitochondrial respiratory metabolism in the light. Invoking the Kok effect in plant physiology models should improve our ability to simulate carbon fluxes of terrestrial ecosystems.