The study integrated genetic architecture derived from maize GWAS into phenotypic simulations of hybrid populations, using ≥200 top GWAS hits and adjusting marker effect sizes, which increased the correlation between simulated and empirical trait data across environments (r = 0.397–0.915). These informed simulations produced realistic trait distributions and genomic prediction results that closely matched empirical observations, demonstrating improved utility for digital breeding programs.

The study reveals that the plant immune regulator NPR1 is modulated by opposing post‑translational modifications mediated by the nutrient‑sensing kinases TOR and SnRK1. Under normal conditions TOR phosphorylates NPR1 at Ser‑55/59 to suppress its activity, while salicylic‑acid‑induced SnRK1 activation inhibits TOR and phosphorylates NPR1 at Ser‑557, thereby activating NPR1 and linking metabolic status to immune signaling.

The study shows that the SnRK1 catalytic subunit KIN10 directs tissue-specific growth‑defense programs in Arabidopsis thaliana by reshaping transcriptomes. kin10 knockout mutants exhibit altered root transcription, reduced root growth, and weakened defense against Pseudomonas syringae, whereas KIN10 overexpression activates shoot defense pathways, increasing ROS and salicylic acid signaling at the cost of growth.

The study examined early metabolic responses to salt stress in a salt‑tolerant alfalfa cultivar, focusing on SnRK1 activity, sucrose, and trehalose‑6‑phosphate dynamics during leaf expansion. Hydroponically grown plants exposed to 200 mM NaCl showed rapid, wave‑like SnRK1 activation within 1 hour, a transient decline in chloroplast performance, and an uncoupling of the Tre6P‑sucrose regulatory link, with a second SnRK1 peak correlating with reduced leaf growth. Exogenous sucrose inhibited SnRK1 activity, highlighting early SnRK1 activation as a pivotal component of salt stress adaptation.

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 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.