The study investigates the role of the SNF1-related kinase 1 (SnRK1) in conferring quantitative resistance to clubroot disease caused by Plasmodiophora brassicae in Arabidopsis thaliana. Increased nuclear SnRK1 activity suppresses disease development by down‑regulating sucrose transporter and cell wall invertase expression and activity, thereby reducing sink strength, while the pathogen effector PBZF1 interferes with SnRK1 nuclear translocation.

The study examined how DNA methylation influences cold stress priming in Arabidopsis thaliana, revealing that primed plants exhibit distinct gene expression and methylation patterns compared to non-primed plants. DNA methylation mutants, especially met1 lacking CG methylation, showed altered cold memory and misregulation of the CBF gene cluster, indicating that methylation ensures transcriptional precision during stress recall.

The study demonstrates that trehalose‑6‑phosphate (T6P), a sucrose‑derived metabolite, acts as the central signal linking carbon availability to Target of Rapamycin (TOR) activation in plants. Using Arabidopsis and Brassica napus, the authors show that T6P is necessary for sucrose‑induced TOR activity and that it counteracts SnRK1‑mediated inhibition of TOR, establishing a sucrose‑T6P‑SnRK1‑TOR signaling axis that promotes cell growth.

A comprehensive multi‑environment trial of 437 maize testcross hybrids derived from 38 MLN‑tolerant lines and 29 testers identified additive genetic effects as the primary driver of grain yield, disease resistance, and drought tolerance. Strong general combining ability and specific combining ability patterns were uncovered, with top hybrids delivering up to 5.75 t ha⁻¹ under MLN pressure while maintaining high performance under optimum and drought conditions. The study provides a framework for selecting elite parents and exploiting both additive and non‑additive effects to develop resilient maize hybrids for sub‑Saharan Africa.

The study demonstrates that the plastid chaperone CLPC2, but not its paralogue CLPC1, is essential for Arabidopsis responsiveness to microbial volatile compounds and for normal seed and seedling development. Loss of CLPC2 alters the chloroplast proteome, affecting proteins linked to growth, photosynthesis, and embryogenesis, while overexpression of CLPC2 mimics CLPC1 deficiency, highlighting distinct functional roles within the CLP protease complex.

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 reveals that the energy sensor SnRK1 modulates Arabidopsis defense by repressing SA‑dependent gene expression and bacterial resistance, with its activity enhanced under high humidity. SnRK1 interacts with TGA transcription factors to attenuate PR1 expression, linking cellular energy status to immune regulation.

The study used CRISPR/Cas9 to generate rice snrk1 mutants and performed integrated phenotypic, transcriptomic, proteomic, and phosphoproteomic analyses under normal and starvation conditions, revealing SnRK1’s dual role in promoting growth and mediating stress responses. Findings indicate sub-functionalization of SnRK1 subunits and identify novel phosphorylation targets linked to membrane trafficking, ethylene signaling, and ion transport.

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.