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 examined the roles of AtKUP2, AtKUP6, AtKUP8, and GORK potassium transport proteins in guard cell function by performing gas-exchange measurements on mature Arabidopsis leaves. Loss of KUP2/6/8 reduced stomatal conductance, whereas a GORK loss‑of‑function mutant showed increased conductance, yet the magnitude of light‑ and ABA‑induced transpiration changes remained similar across genotypes, suggesting a limited dynamic range for rapid stomatal movements that relies on small ionic osmolytes.

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 shows that Arabidopsis root tips adapt to hypoxia by increasing H3K4me3 levels, linked to the inhibition of group 7 demethylases (KDM7s). Genetic loss of KDM7s mimics hypoxic conditions, activating genes that sustain meristem survival, suggesting KDM7s act as root‑specific oxygen sensors that prime epigenetic tolerance mechanisms.

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 reveals that the methyl‑CpG‑binding domain protein MBD8 interacts with the histone demethylase LDL2 to facilitate removal of H3K4me1 and transcriptional repression downstream of H3K9me2 in Arabidopsis. MBD8 binds GC‑poor DNA independently of cytosine methylation and stabilizes LDL2 protein levels, indicating a broader role for MBD proteins beyond methyl‑DNA recognition.

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 used chemically induced effector-triggered immunity combined with single-cell transcriptomics to map immune responses across all leaf cell types in Arabidopsis, revealing that while a core defense program is universally activated, individual cell types deploy distinct transcriptional modules. Functional assays showed that epidermis‑specific transcriptional regulators are essential for preventing pathogen penetration, indicating a spatial division of immune functions within the leaf.

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.