Genetius

The study identifies the cysteine‑rich receptor‑like kinase CRK5 as a negative regulator of salicylic‑acid‑mediated cell death and a positive regulator of antioxidant homeostasis during dark‑induced leaf senescence in Arabidopsis. Loss‑of‑function crk5 mutants display accelerated senescence, elevated ROS and electrolyte leakage, and altered antioxidant enzyme activities, phenotypes that are rescued by suppressing SA biosynthesis or catabolism. Transcriptome analysis reveals extensive deregulation of senescence‑ and redox‑related genes, highlighting CRK5’s central role in coordinating hormonal and oxidative pathways.

The study demonstrates that the plastid chaperone CLPC2, but not its paralogue CLPC1, is essential for Arabidopsis responsiveness to microbial volatile compounds and for normal seed and seedling development. Loss of CLPC2 alters the chloroplast proteome, affecting proteins linked to growth, photosynthesis, and embryogenesis, while overexpression of CLPC2 mimics CLPC1 deficiency, highlighting distinct functional roles within the CLP protease complex.

The study demonstrates that FERONIA and phytochrome B physically interact with the NADPH oxidase RBOHD, and that FERONIA-mediated phosphorylation of phyB is essential for RBOHD-driven ROS production under excess light stress in Arabidopsis thaliana. Additional membrane proteins CRK10 and PIP2;6 also associate with this complex, forming a plasma‑membrane assembly that integrates multiple signaling pathways to regulate stress‑induced ROS.

The study integrates multi-omics data from six Sorghum bicolor accessions under field drought to link RNA covalent modifications (RCMs) with photosynthetic performance, identifying the enzyme SbDUS2 that produces dihydrouridine (DHU) on transcripts. Loss‑of‑function dus2 mutants in Arabidopsis thaliana reveal that DHU deficiency leads to hyperstability of photosynthesis‑related mRNAs, impairing germination, development, and stress‑induced CO2 assimilation. The authors propose DHU as a post‑transcriptional mark that promotes rapid mRNA turnover during abiotic stress, enhancing plant resilience.

The study examined how Arabidopsis calcium‑dependent protein kinases AtCPK5 and AtCPK6 modulate immunity triggered by bacterial rhamnolipids, finding that RLs up‑regulate these kinases and that mutants, especially cpk5/6, show altered reactive oxygen species production and defense gene expression. However, these kinases did not influence RL‑induced electrolyte leakage or resistance to Pseudomonas syringae pv. tomato DC3000, indicating additional signaling components are involved.

A comparative phosphoproteomics study using Arabidopsis thaliana ahk5 loss‑of‑function mutants and wild‑type seedlings revealed that the histidine kinase AHK5 mediates a rapid shift from multistep phosphorelay signaling to serine/threonine phosphorylation in response to H2O2. AHK5 controls ROS‑responsive phosphorylation of plasma‑membrane nanodomain proteins and orchestrates distinct ABA‑independent stomatal closure and ABA‑dependent root development pathways by modulating key components such as RBOHD, CAS, HPCA1, and auxin transporters.

The study introduces a native‑condition method combining cell fractionation and immuno‑isolation to purify autophagic compartments from Arabidopsis, followed by proteomic and lipidomic characterisation of the isolated phagophore membranes. Proteomic profiling identified candidate proteins linked to autophagy, membrane remodeling, vesicular trafficking and lipid metabolism, while lipidomics revealed a predominance of glycerophospholipids, especially phosphatidylcholine and phosphatidylglycerol, defining the unique composition of plant phagophores.

The study resolves the ectodomain structure of the plant-specific LRR‑RLK CARD1 (HPCA1) and reveals a surface‑exposed copper ion coordinated by histidines that is essential for hydrogen peroxide signaling. Combined structural, genetic, and biochemical analyses show that previously identified cysteine residues are not required for signal perception, establishing CARD1 as the first copper‑dependent redox receptor.

The study reconstitutes Papaver rhoeas self‑incompatibility (SI) in Arabidopsis thaliana by expressing the pollen S‑determinant PrpS, revealing that SI triggers a rapid Ca2+‑dependent signaling cascade that leads to mitochondrial H2O2 production, metabolic collapse, and programmed cell death. Using a genetically encoded H2O2 sensor and metabolic assays, the authors show that early mitochondrial disruption, driven by altered Ca2+, cytosolic pH, and distinct ROS sources, is central to the SI response.

The authors established a live‑cell imaging platform that combines confocal microscopy of genetically encoded fluorescent protein biosensors with on‑stage illumination to monitor pH, MgATP²⁻, and NADH/NAD⁺ dynamics during dark‑light transitions in Arabidopsis mesophyll cells. They discovered that photosynthetic proton pumping triggers a stromal alkalinization wave extending to the cytosol and mitochondria, elevates MgATP²⁻ levels, and drives reduction of the NAD pool, with malate dehydrogenase mutants showing altered cytosolic redox even in darkness. This methodological advance enables high‑resolution mapping of photosynthesis‑linked energy physiology across cellular compartments.