Extensive research revealed tremendous details about how plants sense pathogen effectors during effector-triggered immunity (ETI). However, less is known about downstream signaling events. In this report, we demonstrate that prolonged activation of MPK3 and MPK6, two Arabidopsis pathogen-responsive mitogen-activated protein kinases (MPKs), is essential to ETI mediated by both coiled coil-nucleotide binding site-leucine rich repeats (CNLs) and toll/interleukin-1 receptor nucleotide binding site-leucine rich repeats (TNLs) types of R proteins. MPK3/MPK6 activation rapidly alters the expression of photosynthesis-related genes and inhibits photosynthesis, which promotes the accumulation of superoxide ( ) and hydrogen peroxide (H₂O₂), two major reactive oxygen species (ROS), in chloroplasts under light. In the chemical-genetically rescued mpk3 mpk6 double mutants, ETI-induced photosynthetic inhibition and chloroplastic ROS accumulation are compromised, which correlates with delayed hypersensitive response (HR) cell death and compromised resistance. Furthermore, protection of chloroplasts by expressing a plastid-targeted cyanobacterial flavodoxin (pFLD) delays photosynthetic inhibition and compromises ETI. Collectively, this study highlights a critical role of MPK3/MPK6 in manipulating plant photosynthetic activities to promote ROS accumulation in chloroplasts and HR cell death, which contributes to the robustness of ETI. Furthermore, the dual functionality of MPK3/MPK6 cascade in promoting defense and inhibiting photosynthesis potentially allow it to orchestrate the trade-off between plant growth and defense in plant immunity. Plants follow different strategies to defend themselves against pathogens and activate their immune systems once the pathogens have been detected. One of the responses observed is the inhibition of photosynthesis and the global down-regulation of genes that regulate this process, similar to what is frequently observed in plants under various biotic stress conditions. However, the mechanisms underlying the turning off of the photosynthetic activity and whether this process contributes to plants’ defense against pathogens remain to be determined. In this study, we analyze these mechanisms in Arabidopsis plants and show that prolonged activation of MPK3 and MPK6, two kinases critical for pathogen resistance, results in the inhibition of photosynthesis and accumulation of reactive oxygen species (ROS) in the chloroplasts. We find that this response is similar to that observed during pathogen effector-triggered immunity (ETI). Correspondingly, plants that carry mutant versions of MPK3 and MPK6 result in compromised ETI-induced photosynthetic inhibition and chloroplastic ROS accumulation; thus, these two kinases seem to be essential for ETI. Our results suggest that MPK3/MPK6 activation induces a global down-regulation of photosynthesis along with an up-regulation of defense-related genes, and coordinates the growth and defense trade-off in plants.

In land plants, the NAD(P)H dehydrogenase (NDH) complex reduces plastoquinones and drives cyclic electron flow (CEF) around PSI. It also produces extra ATP for photosynthesis and improves plant fitness under conditions of abiotic environmental stress. To elucidate the role of CEF in salt tolerance of the photosynthetic apparatus, Na⁺ concentration, chlorophyll fluorescence, and expression of NDH B and H subunits, as well as of genes related to cellular and vacuolar Na⁺ transport, were monitored. The salt-tolerant Glycine max (soybean) variety S111-9 exhibited much higher CEF activity and ATP accumulation in light than did the salt-sensitive variety Melrose, but similar leaf Na⁺ concentrations under salt stress. In S111-9 plants, ndhB and ndhH were highly up-regulated under salt stress and their corresponding proteins were maintained at high levels or increased significantly. Under salt stress, S111-9 plants accumulated Na⁺ in the vacuole, but Melrose plants accumulated Na⁺ in the chloroplast. Compared with Melrose, S111-9 plants also showed higher expression of some genes associated with Na⁺ transport into the vacuole and/or cell, such as genes encoding components of the CBL10 (calcineurin B-like protein 10)–CIPK24 (CBL-interacting protein kinase 24)–NHX (Na⁺/H⁺ antiporter) and CBL4 (calcineurin B-like protein 4)–CIPK24–SOS1 (salt overly sensitive 1) complexes. Based on the findings, it is proposed that enhanced NDH-dependent CEF supplies extra ATP used to sequester Na⁺ in the vacuole. This reveals an important mechanism for salt tolerance in soybean and provides new insights into plant resistance to salt stress.

The physiological response of two soybean varieties to salt stress was examined. The results showed that salt stress induced a significantly (p<0.01) lower decrease of the net photosynthetic rate (P _N) in salt-tolerant S111-9 than in salt-sensitive Glycine max. P _N decrease was positively related to the decrease of stomatal conductance (g _s) and intercellular CO₂ concentration (C _i) in S111-9, while with g _s in G. max. a threshold of relative water content (RWC) was found, above which a slight decrease in RWC lead to a sharp reduction in g _s. The photochemical quenching (q_P), the efficiency of open PSII centers (Φ_PSII) and the Rubisco activity (RA) significantly decreased with increasing salinity level in G. max. The maximum PSII quantum yield (F_v/F_m) decreased significantly under the highest NaCl in both varieties. The higher reduction of RA in G. max was attributed to Rubisco content, which was mainly regulated at LSU expression level rather than at rbcL transcript level. These findings led us to conclude that the salt-induced reduction in P _N was mainly due g _s and RA for S111-9 and G. max, respective

Ribulose-1,5-bisphosphate carboxylase/oxygenase activase (RCA) is a nuclear gene that encodes a chloroplast protein that plays an important role in photosynthesis. Some reports have indicated that it may play a role in acclimation to different abiotic stresses. In this paper, we analyzed the stress-responsive elements in the 2.0 kb 5’-upstream regions of the RCA gene promoter and the primary, secondary and tertiary structure of the protein. We identified some cis-elements of multiple stress-related components in the RCA promoter. Amino acid and evolution analyses showed that the RCA protein had conserved regions between different species; however, the size and type varied. The secondary structures, binding sites and tertiary structures of the RCA proteins were also different. This might reflect the differences in the transcription and translation levels of the two RCA isoforms during adaptation to different abiotic stresses. Although both the transcription and translation levels of RCA isoforms in the rice leaves increased under various stresses, the large isoform was increased more significantly in the chloroplast stroma and thylakoid. It can be concluded that RCA, especially RCA_L, is also a multiple responder to abiotic stresses in rice, which provides new insights into RCA functions.