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.

Summary: In flowering plants, developing embryos reside in maternal sporophytes. It is known that maternal generation influences the development of next‐generation embryos; however, little is known about the signaling components in the process. Previously, we demonstrated that Arabidopsis mitogen‐activated protein kinase 6 (MPK6) and MPK3 play critical roles in plant reproduction. In addition, we noticed that a large fraction of seeds from mpk6 single‐mutant plants showed a wrinkled seed coat or a burst‐out embryo phenotype. Here, we report that these seed phenotypes can be traced back to defective embryogenesis. The defective embryos have shorter suspensors and reduced growth along the longitudinal axis. Furthermore, the cotyledons fail to bend over to progress to the bent‐cotyledon stage. As a result of the uneven circumference along the axis, the seed coat wrinkles to develop raisin‐like morphology after dehydration. In more severe cases, the embryo can be pushed out from the micropylar end, resulting in the burst‐out embryo seed phenotype. Genetic analyses demonstrated that the defective embryogenesis of the mpk6 mutant is a maternal effect. Heterozygous or homozygous mpk6 embryos have defects only in mpk6 homozygous maternal plants, but not in wild‐type or heterozygous maternal plants. The loss of function of MKK4/MKK5 also results in the same phenotypes, suggesting that MKK4/MKK5 might act upstream of MPK6 in this pathway. The maternal‐mediated embryo defects are associated with changes in auxin activity maxima and PIN localization. In summary, this research demonstrates that the Arabidopsis MKK4/MKK5–MPK6 cascade is an important player in the maternal control of embryogenesis.

Arabidopsis WRKY15 functions upstream of VND7, an important regulator of tracheary element (TE) differentiation, to suppress TE formation during plant vascular

A cDNA library generated from seeds of Cassia obtusifolia was sequenced using Illumina/Solexa platform. More than 12,968,231 high quality reads were generated, and have been deposited in NCBI SRA (SRR 1012912). A total of 40,102 unigenes (>200 bp) were obtained with an average sequence length of 681 bp by de novo assembly. About 34,089 (85%) unique sequences were annotated and 8694 of the unique sequences were assigned to specific metabolic pathways by the Kyoto Encyclopedia of Genes and Genomes. Among them, 131 unigenes, which are involved in the biosynthesis and (or) regulation of anthraquinone, carotenoid, flavonoid, and lipid, the 4 best known active metabolites, were identified from cDNA library. In addition, three lipid transfer proteins were obtained, which may contribute to the lipid molecules transporting between biological membranes. Meanwhile, 30 cytochrome P450, 12 SAM-dependent methyltransferases, and 12 UDP-glucosyltransferase unigenes were identified, which could also be responsible for the biosynthesis of active metabolites.