The study engineers Type‑B response regulators to alter their transcriptional activity and cytokinin sensitivity, enabling precise modulation of cytokinin‑dependent traits. Using tissue‑specific promoters, the synthetic transcription factors were deployed in Arabidopsis thaliana to reliably increase or decrease lateral root numbers, demonstrating a modular platform for controlling developmental phenotypes.

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 examines how the SnRK1 catalytic subunit KIN10 integrates carbon availability with root growth regulation in Arabidopsis thaliana. Loss of KIN10 reduces glucose‑induced inhibition of root elongation and triggers widespread transcriptional reprogramming of metabolic and hormonal pathways, notably affecting auxin and jasmonate signaling under sucrose supplementation. These findings highlight KIN10 as a central hub linking energy status to developmental and environmental cues in roots.

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 characterizes the tomato class B heat shock factor SlHSFB3a, revealing its age‑dependent expression in roots and its role in enhancing lateral root density by modulating auxin homeostasis. Overexpression of SlHSFB3a increases lateral root emergence, while CRISPR‑mediated knockouts produce the opposite phenotype, indicating that SlHSFB3a regulates auxin signaling through repression of auxin repressors and activation of the ARF7/LOB20 pathway.