The study shows that maize plants carrying autophagy-defective atg10 mutations exhibit delayed flowering and significant reductions in kernel size, weight, and number, culminating in lower grain yield. Reciprocal crossing experiments reveal that the maternal genotype, rather than the seed genotype, primarily drives the observed kernel defects, suggesting impaired nutrient remobilization from maternal tissues during seed development.

Using the bryophyte Physcomitrium patens, the study shows that loss of autophagy enhances auxin‑driven caulonemata differentiation and colony expansion under low nitrogen or imbalanced carbon/nitrogen conditions, accompanied by higher internal IAA, reduced PpPINA expression, and up‑regulated RSL transcription factors. Autophagy appears to suppress auxin‑induced differentiation during nutrient stress, acting as a hub that balances metabolic cues with hormonal signaling.

Thermopriming enhances heat stress tolerance by orchestrating protein maintenance pathways: it activates the heat shock response (HSR) via HSFA1 and the unfolded protein response (UPR) while modulating autophagy to clear damaged proteins. Unprimed seedlings cannot mount these responses, leading to proteostasis collapse, protein aggregation, and death, highlighting the primacy of HSR and protein maintenance over clearance mechanisms.

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 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.

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.