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Chloroplasts use light energy and a linear electron transport (LET) pathway for the coupled generation of NADPH and ATP. It is widely accepted that the production ratio of ATP to NADPH is usually less than required to fulfill the energetic needs of the chloroplast. Left uncorrected, this would quickly result in an over-reduction of the stromal pyridine nucleotide pool (i.e., high NADPH/NADP+ ratio) and under-energization of the stromal adenine nucleotide pool (i.e., low ATP/ADP ratio). These imbalances could cause metabolic bottlenecks, as well as increased generation of damaging reactive oxygen species. Chloroplast cyclic electron transport (CET) and the chloroplast malate valve could each act to prevent stromal over-reduction, albeit in distinct ways. CET avoids the NADPH production associated with LET, while the malate valve consumes the NADPH associated with LET. CET could operate by one of two different pathways, depending upon the chloroplast ATP demand. The NADH dehydrogenase-like pathway yields a higher ATP return per electron flux than the pathway involving PROTON GRADIENT REGULATION5 (PGR5) and PGR5-LIKE PHOTOSYNTHETIC PHENOTYPE1 (PGRL1). Similarly, the malate valve could couple with one of two different mitochondrial electron transport pathways, depending upon the cytosolic ATP demand. The cytochrome pathway yields a higher ATP return per electron flux than the alternative oxidase (AOX) pathway. In both Arabidopsis thaliana and Chlamydomonas reinhardtii, PGR5/PGRL1 pathway mutants have increased amounts of AOX, suggesting complementary roles for these two lesser-ATP yielding mechanisms of preventing stromal over-reduction. These two pathways may become most relevant under environmental stress conditions that lower the ATP demands for carbon fixation and carbohydrate export.

Plant carbon balance depends upon the difference between photosynthetic carbon gain and respiratory carbon loss. In C 3 plants, growth at an elevated atmospheric concentration of CO 2 (ECO 2 ) stimulates photosynthesis and raises the leaf carbohydrate status, but how respiration responds is less understood. In this study, growth of Nicotiana tabacum at ECO 2 increased the protein amount of the non-energy conserving mitochondrial alternative oxidase (AOX). Growth at ECO 2 increased AOX1a transcript amount, and the transcript amount of a putative sugar-responsive gene encoding a chloroplast glucose-6-phosphate/phosphate translocator (GPT3). We suggest that the elevated amounts of AOX and GPT3 represent distinctive mitochondrial and chloroplast mechanisms to manage an excessive cytosolic pool of sugar phosphates. AOX respiration could consume cytosolic sugar phosphates, without this activity being restricted by rates of ATP turnover. GPT3 could allow accumulating cytosolic glucose-6-phosphate to return to the chloroplast. This could feed starch synthesis or a glucose-6-phosphate shunt in the Calvin cycle. AOX and GPT3 activities could buffer against P i depletions that might otherwise disrupt mitochondrial and chloroplast electron transport chain activities. AOX and GPT3 activities could also buffer against a down-regulation of photosynthetic capacity by preventing a persistent imbalance between photosynthetic carbon gain and the activity of carbon utilizing sinks.

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