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 identifies the extended NT‑C2 domain of Plastid Movement Impaired 1 (PMI1) as the main membrane‑binding module that interacts with PI4P and PI(4,5)P2, requiring basic residues for plasma‑membrane association. Calcium binding by the NT‑C2 domain modulates its phosphoinositide preference, and cytosolic Ca2+ depletion blocks blue‑light‑induced PMI1 redistribution, indicating that both the NT‑C2 domain and adjacent intrinsically disordered regions are essential for PMI1’s role in chloroplast movement.

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 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 uses an optogenetic ChannelRhodopsin 2 variant (XXM2.0) to generate defined cytosolic Ca²⁺ transients in Arabidopsis root cells, revealing that these Ca²⁺ signatures suppress auxin‑induced membrane depolarization, Ca²⁺ spikes, and auxin‑responsive transcription, leading to reversible inhibition of cell division and elongation. This demonstrates that optogenetically imposed Ca²⁺ signals act as dynamic regulators of auxin sensitivity in roots.

The study demonstrates that jasmonate (JA) enhances Arabidopsis thaliana responses to extracellular ATP (eATP) by upregulating the eATP receptor P2K1 and amplifying eATP‑induced cytosolic Ca²⁺ spikes and transcriptional reprogramming in a COI1‑dependent manner, whereas salicylic acid pretreatment suppresses these responses. These findings reveal a JA‑mediated priming mechanism that potentiates eATP signaling during stress.

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 identified a suppressor mutation (sune42) in the Golgi-localized Ca2+ transporter CCX4 that alleviates the dominant‑negative root hair phenotype caused by the extensin‑less LRX1ΔE14 protein in Arabidopsis. Detailed Ca2+ imaging showed that LRX1ΔE14 disrupts tip‑focused cytoplasmic Ca2+ oscillations, a defect rescued by the sune42 mutation, highlighting the role of Golgi‑mediated Ca2+ homeostasis in root hair growth.

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.