Summary Ferns and fern allies have low photosynthetic rates compared with seed plants. Their photosynthesis is thought to be limited principally by physical CO2 diffusion from the atmosphere to chloroplasts. The aim of this study was to understand the reasons for low photosynthesis in species of ferns and fern allies (Lycopodiopsida and Polypodiopsida). We performed a comprehensive assessment of the foliar gas‐exchange and mesophyll structural traits involved in photosynthetic function for 35 species of ferns and fern allies. Additionally, the leaf economics spectrum (the interrelationships between photosynthetic capacity and leaf/frond traits such as leaf dry mass per unit area or nitrogen content) was tested. Low mesophyll conductance to CO2 was the main cause for low photosynthesis in ferns and fern allies, which, in turn, was associated with thick cell walls and reduced chloroplast distribution towards intercellular mesophyll air spaces. Generally, the leaf economics spectrum in ferns follows a trend similar to that in seed plants. Nevertheless, ferns and allies had less nitrogen per unit DW than seed plants (i.e. the same slope but a different intercept) and lower photosynthesis rates per leaf mass area and per unit of nitrogen.

Plant-feeding herbivores can generate complex patterns of foliar wounding, but it is unclear how wounding-elicited volatile emissions scale with the severity of different wounding types, and there is no common protocol for wounding experiments. We investigated the rapid initial response to wounding damage generated by different numbers of straight cuts and punctures through leaf lamina as well as varying area of lamina squeezing in the temperate deciduous tree Populus tremula Wounding-induced volatile emission time-courses were continuously recorded by a proton-transfer-reaction time-of-flight mass-spectrometer. After the mechanical wounding, an emission cascade was rapidly elicited resulting in sequential emissions of key stress volatiles methanol, acetaldehyde, and volatiles of the lipoxygenase pathway, collectively constituting more than 97% of the total emission. The maximum emission rates, reached after one to three minutes after wounding, and integrated emissions during the burst were strongly correlated with the severity in all damage treatments. For straight cuts and punch hole treatments, the emissions per cut edge length were constant, indicating a direct proportionality. Our results are useful for screening wounding-dependent emission capacities.

Brassicales released volatile glucosinolate breakdown products upon tissue mechanical damage, but it is unclear how glucosinolate volatile release responds to abiotic stresses such as heat stress. We used three different heat treatments called as mild -and long-term stress and shock-heating to gain insight into stress-dependent changes in volatile blends and photosynthetic characteristics in Brassica nigra (L.) Koch. The reduction in net assimilation rate (A) in temperature response curve measurements was associated with decreases in stomatal conductance, while the moderate reduction due to long-term stress after exposure to 40-44 °C and collapse of photosynthetic activity after heat shock stress were associated with non-stomatal processes. Mild stress decreased constitutive monoterpene emissions parallel to photosynthesis, while long-term heat stress at 40-44 °C and heat shock stress resulted the emissisons of lipoxygenase (LOX) pathway and glucosinolate volatiles. However, glucosinolate volatile emission was more strongly elicited by long-term stress, and glucosinolate volatiles dominated the emissions in long-term stressed plants, while LOX products dominated the emissions after heat shock. These results demonstrate that glucosinolate volatiles constitute a major part of emission blend in heat-stressed B. nigra plants, especially upon chronic stress that leads to induction responses.

Recently, a feedback inhibition of the chloroplastic 1-deoxy-D-xylulose 5-phosphate (DXP)/2-C-methyl-D-erythritol 4-phosphate (MEP) pathway of isoprenoid synthesis by end products dimethylallyl diphosphate (DMADP) and isopentenyl diphosphate (IDP) was postulated, but the extent to which DMADP and IDP can build up is not known. We used bisphosphonate inhibitors, alendronate and zoledronate, that inhibit the consumption of DMADP and IDP by prenyltransferases to gain insight into the extent of end product accumulation and possible feedback inhibition in isoprene-emitting hybrid aspen (Populus tremula 3 Populus tremuloides). A kinetic method based on dark release of isoprene emission at the expense of substrate pools accumulated in light was used to estimate the in vivo pool sizes of DMADP and upstream metabolites. Feeding with fosmidomycin, an inhibitor of DXP reductoisomerase, alone or in combination with bisphosphonates was used to inhibit carbon input into DXP/MEP pathway or both input and output. We observed a major increase in pathway intermediates, 3-to 4-fold, upstream of DMADP in bisphosphonateinhibited leaves, but the DMADP pool was enhanced much less, 1.3-to 1.5-fold. In combined fosmidomycin/bisphosphonate treatment, pathway intermediates accumulated, reflecting cytosolic flux of intermediates that can be important under strong metabolic pull in physiological conditions. The data suggested that metabolites accumulated upstream of DMADP consist of phosphorylated intermediates and IDP. Slow conversion of the huge pools of intermediates to DMADP was limited by reductive energy supply. These data indicate that the DXP/MEP pathway is extremely elastic, and the presence of a significant pool of phosphorylated intermediates provides an important valve for fine tuning the pathway flux.

Measurements of 810 nm transmittance changes in leaves, simultaneously with Chl fluorescence, CO(2) uptake and O(2) evolution, were carried out on potato (Solanum tuberosum L.) leaves with altered expression of plastidic NADP-dependent malate dehydrogenase. Electron transport rates were calculated: J(C) from the CO(2) uptake rate considering ribulose-1,5-bisphosphate (RuBP) carboxylation and oxygenation, J(O) from the O(2) evolution rate, J(F) from Chl fluorescence parameters and J(I) from the post-illumination re-reduction speed of PSI donors. In the absence of external O(2), J(O) equaled (1.005 +/- 0.003) J(C), independent of the transgenic treatment, light intensity and CO(2) concentration. This showed that nitrite and oxaloacetate reduction rates were very slow. The Mehler-type O(2) reduction was evaluated from the rate of electron accumulation at PSI after the O(2) concentration was decreased from 210 to 20 mmol mol(-1), and resulted in <1% of the linear flow. J(F) and J(I) did not differ from J(C) while photosynthesis was light-limited, but considerably exceeded J(C) at saturating light. Then, typically, J(F) = 1.2 J(C) and J(I) = 1.3 J(C), and J(F) -J(C) and J(I) -J(C) depended little on CO(2) and O(2) concentrations. The results showed that the alternative and cyclic electron flow necessary to compensate variations in the ATP/NADPH ratio were only a few percent of the linear flow. The data do not support the requirement of 14H(+)/3ATP by the chloroplast ATP synthase. We suggest that the fast PSI cyclic electron flow J(I) - J(C), as well as the fast J(F) - J(C) are energy-dissipating cycles around PSI and PSII at light saturation.