Plants lacking OST1 show conditional stomatal closure and wildtype-like growth sensitivity at high VPD.

Climate change-associated rise in VPD (atmospheric vapor pressure deficit) results in increased plant transpiration and reduced stomatal conductance, photosynthesis, biomass, and yield. High VPD-induced stomatal closure of Arabidopsis is an active process regulated via the kinase SnRK2.6 (OPEN STOMATA 1, OST1). Here, we performed gas exchange, leaf water potential and rosette growth measurements to study, whether (1) high VPD-induced stomatal closure is detected in plants carrying loss-of-function mutations in OST1 (ost1-3) when they are grown at reduced soil water content or measured at increased air temperature; (2) ost1-3 plants expressing OST1 construct with no ABA-activation domain, but intact ABA-independent activation, show stronger stomatal VPD response compared with ost1-3 plants; and (3) rosette area and biomass of ost1-3 are more affected by growth at high VPD compared with Col-0. The stomata of well-watered ost1-3 plants were insensitive to high VPD regardless of air temperature, but in deficit-irrigated ost1-3, leaf water potential decreased the most and stomata closed at high VPD. Differences between VPD-induced stomatal closures of ost1-3 plants and ost1-3 plants expressing OST1 with no ABA-activation domain point at gradual VPD-induced ABA-independent activation of OST1. High VPD conditions led to similar reductions in rosette area and specific leaf area of well-watered Col-0 and ost1-3 plants. Rosette dry mass was unaffected by high VPD. Our results show that OST1 loss-of-function plants display conditional stomatal closure and no extra sensitivity of rosette area growth compared with Col-0 wildtype under high VPD conditions.

Evidence that light, carbon dioxide, and oxygen dependencies of leaf isoprene emission are driven by energy status in hybrid aspen.

Leaf isoprene emission scales positively with light intensity, is inhibited by high carbon dioxide (CO(2)) concentrations, and may be enhanced or inhibited by low oxygen (O(2)) concentrations, but the mechanisms of environmental regulation of isoprene emission are still not fully understood. Emission controls by isoprene synthase, availability of carbon intermediates, or energetic cofactors have been suggested previously. In this study, we asked whether the short-term (tens of minutes) environmental control of isoprene synthesis results from alterations in the immediate isoprene precursor dimethylallyldiphosphate (DMADP) pool size, and to what extent DMADP concentrations are affected by the supply of carbon and energetic metabolites. A novel in vivo method based on postillumination isoprene release was employed to measure the pool size of DMADP simultaneously with the rates of isoprene emission and net assimilation at different light intensities and CO(2) and O(2) concentrations. Both net assimilation and isoprene emission rates increased hyperbolically with light intensity. The photosynthetic response to CO(2) concentration was also hyperbolic, while the CO(2) response curve of isoprene emission exhibited a maximum at close to CO(2) compensation point. Low O(2) positively affected both net assimilation and isoprene emission. In all cases, the variation in isoprene emission was matched with changes in DMADP pool size. The results of these experiments suggest that DMADP pool size controls the response of isoprene emission to light intensity and to CO(2) and O(2) concentrations and that the pool size is determined by the level of energetic metabolites generated in photosynthesis.