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 authors used a bottom‑up thermodynamic modelling framework to investigate how plants decode calcium signals, starting from Ca2+ binding to EF‑hand proteins and extending to higher‑order decoding modules. They identified six universal Ca2+-decoding modules that can explain variations in calcium sensitivity among kinases and provide a theoretical basis for interpreting calcium signal amplitude and frequency in plant cells.

The study reveals that rice perceives Xanthomonas oryzae pv. oryzae outer membrane vesicles through a rapid calcium signal that triggers plasma‑membrane nanodomain formation and the re‑organisation of defence‑related proteins, establishing an early immune response. Without this Ca2+ signal, OMVs are not recognized and immunity is weakened.

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 identifies wound‑induced proline transporters ProT2 and ProT3 as central regulators that link salicylic acid signaling to the suppression of de novo root regeneration (DNRR) via modulation of reactive oxygen species dynamics. Genetic loss of these transporters or pharmacological inhibition of proline transport alleviates SA‑mediated regeneration inhibition across several plant species without compromising disease resistance.

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.

Using a microfluidic valve rootchip, the study simultaneously tracked ROS and calcium dynamics in compressed roots and found three kinetic phases linking mechanosensitive channel activity, NADPH oxidase‑dependent ROS accumulation, and secondary calcium influx. Pharmacological inhibition revealed that a fast calcium response is mediated by plasma‑membrane mechanosensitive channels, while a slower calcium increase is driven by ROS production.

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.