ENDOGENOUS INORGANIC CARBON SOURCES IN PLANT PHOTOSYNTHESIS

I. OCCURRENCE OF THE DARK RESPIRATORY PATHWAYS IN ILLUMINATED GREEN CELLS

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Summary

The biochemical evidence concerning the rate of production of CO2 by dark respiratory pathways in illuminated green plant cells is reviewed.

Pyruvate decarboxylation and the TCAC are important sources of biosynthetic intermediates in the light as well as in the dark. The rate of CO2 release required to synthesize these carbon skeletons from pyruvate in the light approaches the rate of dark CO2 production. Oxidative phosphorylation, the second important role of the TCAC in the dark, is supplemented and partly replaced by photophosphorylation in the light, and some sort of ‘physiological uncoupling’ may be required to stop the rate of generation of reductant in the TCAC in the light from exceeding the rate of its consumption in oxidative phosphorylation. The decarboxylations of pyruvate and TCAC metabolism occur, in the light as in the dark, in the mitochondria (except possibly in Acetabularia, where they may also occur in the choroplasts). All the decarboxylations produce unhydrated CO2.

The oxidative PPP has no obligatory role to play in carbon skeleton synthesis, and it is supplemented in its dark rôle of NADPH2 synthesis by photoproduction of reductant when the cell is illuminated. Evidence as to whether light stimulates or inhibits the oxidative PPP is contradictory. This pathway occurs in at least some illuminated green cells; the decarboxylation reaction produces unhydrated CO2, and occurs in both the cytoplasm and the chloroplast.

The situation with regard to carbon flux through the dark respiration pathways in various groups of plants is considered quantitatively. Even without taking into account the contribution from light-dependent pathways of CO2 production (photorespiration), it would appear that the absence of net CO2 release to a CO2-free gas stream in the light in a green cell or tissue cannot entirely be attributed to inhibition of respiration. The absence of CO2 release must also reflect the capacity of the tissue for reassimilation of endogenous CO2.

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