Genetius

The study investigated the ability of foliar-applied salicylic acid (SA) to alleviate drought stress in the high‑altitude medicinal plant Valeriana wallichii by measuring physiological and biochemical responses during vegetative and flowering stages. SA at specific concentrations improved photosynthetic rates, water‑use efficiency, chlorophyll content, membrane stability, and root biomass under both severe (25% field capacity) and moderate (50% field capacity) drought conditions. These results suggest that SA treatment enhances drought tolerance and productivity in this species.

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 demonstrates that salicylic acid (SA) restricts plant root growth through a mechanism requiring the transmembrane kinase TMK1, which leads to apoplastic alkalinization and inhibition of plasma membrane H⁺-ATPase phosphorylation. This SA effect operates independently of the auxin receptor ABP1, suggesting a novel SA-mediated pathway that balances stress responses with growth.

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 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.

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.

The study created transgenic Arabidopsis lines enabling inducible plasmodesmal closure via an overactive CALLOSE SYNTHASE3 allele (icals3m) and the C‑terminal domain of PDLP1, independent of pathogen signals. Induced closure triggered stress‑responsive gene expression, elevated salicylic acid levels, and enhanced resistance to Pseudomonas syringae, while also causing starch accumulation, reduced growth, and increased susceptibility to Botrytis cinerea, indicating that plasmodesmal closure itself can activate immune signaling.

The study identified twenty survival of SA-induced death (ssd) mutants that are defective in starch, glucose, nitrate metabolism, and circadian regulation, leading to excessive carbohydrate accumulation and susceptibility to salicylic acid (SA)-induced death in prolonged darkness. Glucose application rescues SA‑treated plants by antagonizing oxidative stress and restoring metabolic balance, as revealed by transcriptomic analyses that link SA‑induced cell death to effector‑triggered immunity pathways.

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.