The study tests whether heavy‑metal stress contributed to maize domestication by exposing teosinte (Zea mays ssp. parviglumis) and the Palomero toluqueno landrace to sublethal copper and cadmium, then analysing genetic diversity, selection signatures, and transcriptomic responses of three chromosome‑5 heavy‑metal response genes (ZmHMA1, ZmHMA7, ZmSKUs5). Results reveal strong positive selection on these genes, heavy‑metal‑induced phenotypes resembling modern maize, and up‑regulation of Tb1, supporting a role for volcanic‑derived metal stress in early maize evolution.

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 examines how ectopic accumulation of methionine in Arabidopsis thaliana leaves, driven by a deregulated AtCGS transgene under a seed‑specific promoter, reshapes metabolism, gene expression, and DNA methylation. High‑methionine lines exhibit increased amino acids and sugars, activation of stress‑hormone pathways, and reduced expression of DNA methyltransferases, while low‑methionine lines show heightened non‑CG methylation without major transcriptional changes. Integrated transcriptomic and methylomic analyses reveal a feedback loop linking sulfur‑carbon metabolism, stress adaptation, and epigenetic regulation.

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.