Phosphite (Phi) and phosphate (Pi) share the same root uptake system, but Phi acts as a biostimulant that modulates plant growth and disease resistance in a species‑ and Pi‑dependent manner. In Arabidopsis, Phi induces hypersensitive‑like cell death and enhances resistance to Plectosphaerella cucumerina, while in rice it counteracts Pi‑induced susceptibility to Magnaporthe oryzae and Fusarium fujikuroi, accompanied by extensive transcriptional reprogramming.
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 evaluated a transgenic soybean line (VPZ-34A) expressing Arabidopsis VDE, PsbS, and ZEP for combined improvements in light‑use efficiency and carbon assimilation under ambient and elevated CO2 in a FACE experiment. While VPZ‑34A showed enhanced maximum quantum efficiency of PSII under fluctuating light, it did not increase carbon assimilation efficiency or yield, and transcriptome analysis revealed limited gene expression changes. The results suggest that VPZ‑mediated photosynthetic gains are insufficient to boost productivity under elevated CO2.
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 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 characterizes a plasma membrane-localized, calcium‑permeable force‑gated channel named Rapid Mechanically Activated (RMA) in plants, using patch‑clamp and pressure‑clamp to elucidate its rapid activation, inactivation, and irreversible adaptation upon repeated mechanical stimulation. Kinetic modeling shows the channel functions as a pass‑band filter for frequencies between 10 Hz and 1 kHz, supporting its role in transducing high‑frequency mechano‑stimuli such as insect vibrations.
The study visualizes subcellular dynamics following activation of the NRC4 resistosome, showing that NRC4 enrichment at the plasma membrane triggers calcium influx, followed by sequential disruption of mitochondria, plastids, endoplasmic reticulum, and cytoskeleton, culminating in plasma membrane rupture and cell death. These observations define a temporally ordered cascade of organelle and membrane events that execute plant immune cell death.