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 introduced full-length SOC1 genes from maize and soybean, and a partial SOC1 gene from blueberry, into tomato plants under constitutive promoters. While VcSOC1K and ZmSOC1 accelerated flowering, all three transgenes increased fruit number per plant mainly by promoting branching, and transcriptomic profiling revealed alterations in flowering, growth, and stress‑response pathways.

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.