The study created a system that blocks root‑mediated signaling between wheat varieties in a varietal mixture and used transcriptomic and metabolomic profiling to reveal that root chemical interactions drive reduced susceptibility to Septoria tritici blotch, with phenolic compounds emerging as key mediators. Disruption of these root signals eliminates both the disease resistance phenotype and the associated molecular reprogramming.

The study characterizes the chloroplast‑localized protein AT4G33780 in Arabidopsis thaliana using CRISPR/Cas9 knockout and overexpression lines, revealing tissue‑specific expression and context‑dependent effects on seed germination, seedling growth, vegetative development, and root responses to nickel stress. Integrated transcriptomic (RNA‑seq) and untargeted metabolomic analyses show extensive transcriptional reprogramming—especially of cell‑wall genes—and altered central energy metabolism, indicating AT4G33780 coordinates metabolic state with developmental regulation rather than controlling single pathways.

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 reveals that REMORIN protein evolution is primarily driven by diversification of their conserved C-terminal domain, defining four major clades. Structural bioinformatics predicts a common membrane‑binding interface with diverse curvatures and lengths, and suggests that some REMs can form C‑terminal‑mediated oligomers, adding complexity to membrane organization.

The study establishes a tractable system using the large bloom-forming diatom Coscinodiscus granii and its natural oomycete parasite Lagenisma coscinodisci, enabling manual isolation of single host cells and stable co-cultures. High‑quality transcriptomes for both partners were assembled, revealing diverse oomycete effectors and a host transcriptional response involving proteases and exosome pathways, while also profiling the co‑occurring heterotrophic flagellate Pteridomonas sp. This tripartite platform provides a unique marine model for dissecting molecular mechanisms of oomycete‑diatom interactions.

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.