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 introduced charge-altering mutations into the N‑terminal region of Lhcb2 in Arabidopsis thaliana lacking native Lhcb2 to assess how intrinsic charge affects LHCII phosphorylation, state‑transition efficiency, and PSI‑LHCII complex formation. The R2E mutation drastically reduced Lhcb1/2 phosphorylation, impaired state transitions, and prevented PSI‑LHCII assembly, whereas the Q9E mutation had no measurable impact, and neither mutation altered thylakoid ultrastructure. Residual state transitions in the R2E line suggest that other Stn7 substrates can partially compensate for the loss of Lhcb2 phosphorylation.

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 compares the iron-poor oceanic diatom Thalassiosira oceanica with the iron-rich coastal species T. pseudonana to uncover how diatoms adapt to low-iron conditions. Using photo‑physiological measurements, proteomic profiling, and focused ion beam scanning electron microscopy, the researchers show that each species remodels chloroplast compartments and exhibits distinct mitochondrial architectures to maintain chloroplast‑mitochondrial coupling under iron limitation.

The study demonstrates that the plastid chaperone CLPC2, but not its paralogue CLPC1, is essential for Arabidopsis responsiveness to microbial volatile compounds and for normal seed and seedling development. Loss of CLPC2 alters the chloroplast proteome, affecting proteins linked to growth, photosynthesis, and embryogenesis, while overexpression of CLPC2 mimics CLPC1 deficiency, highlighting distinct functional roles within the CLP protease complex.

The authors compiled and standardized published data on Rubisco dark inhibition for 157 flowering plant species, categorizing them into four inhibition levels and analyzing phylogenetic trends. Their meta‑analysis reveals a complex, uneven distribution of inhibition across taxa, suggesting underlying chloroplast microenvironment drivers and providing a new resource for future photosynthesis improvement efforts.

The study investigated how barley (Hordeum vulgare) adjusts mitochondrial respiration under salinity stress using physiological, biochemical, metabolomic and proteomic approaches. Salt treatment increased respiration and activated the canonical TCA cycle, while the GABA shunt remained largely inactive, contrasting with wheat responses.

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 reveals that brassinosteroids activate phosphoenolpyruvate carboxykinase (PCK) by promoting dephosphorylation of conserved Ser-62 and Thr-66 residues, a process antagonized by the GSK3-like kinase BIN2. BR‑deficient Arabidopsis mutants exhibit reduced PCK activity, while phospho‑blocking mutations confer BR‑independent activation and enhanced seedling growth, and similar regulatory mechanisms are observed in maize and sorghum leaves.