The study compared physiological, ion‑balance, and metabolic responses of two maize inbred lines—salt‑sensitive C68 and salt‑tolerant NC326—under salinity stress. Untargeted metabolomics identified 56 metabolites and, together with genetic analysis, linked 10 candidate genes to key protective metabolites, revealing constitutive and inducible mechanisms of salt tolerance.

The study models maize flowering time plasticity using a physiological reaction norm derived from multi-environment trial data, revealing genotype-specific differences in temperature-driven development and photoperiod perception. It introduces an envirotyping metric that shows genotypes can experience markedly different photoperiods even within the same environment, and demonstrates distinct adaptive strategies between tropical and temperate germplasm.

The study employed a multi‑omics workflow (transcriptomics, ribosome profiling, and proteomics) to uncover small peptides encoded by long non‑coding RNAs (LSEPs) in rice, finding that over 40% of surveyed lncRNAs associate with ribosomes. An optimized small‑peptide extraction followed by LC‑MS/MS identified 403 LSEPs, confirming the peptide‑coding capacity of plant lncRNAs and providing a scalable pipeline for large‑scale screening.

The study generated a temporal physiological and metabolomic map of leaf senescence in diverse maize inbred lines differing in stay‑green phenotype, identifying 84 metabolites associated with senescence and distinct metabolic signatures between stay‑green and non‑stay‑green lines. Integration of metabolite data with genomic information uncovered 56 candidate genes, and reverse‑genetic validation in maize and Arabidopsis demonstrated conserved roles for phenylpropanoids such as naringenin chalcone and eriodictyol in regulating senescence.

The study investigated unexpected leaf spot symptoms in Psa3‑resistant kiwifruit (Actinidia) germplasm, finding that Psa3 was detectable by qPCR and metabarcoding despite poor culturing. Metabarcoding revealed distinct bacterial community shifts in lesions versus healthy tissue, and whole‑genome sequencing identified diverse Pseudomonas spp. that, while not individually more pathogenic, could enhance Psa3 growth, suggesting pathogenic consortia on resistant hosts.