Phosphite (Phi) and phosphate (Pi) share the same root uptake system, but Phi acts as a biostimulant that modulates plant growth and disease resistance in a species‑ and Pi‑dependent manner. In Arabidopsis, Phi induces hypersensitive‑like cell death and enhances resistance to Plectosphaerella cucumerina, while in rice it counteracts Pi‑induced susceptibility to Magnaporthe oryzae and Fusarium fujikuroi, accompanied by extensive transcriptional reprogramming.

The study generated a dataset of 420 sgRNAs targeting promoters, exons, and introns of 137 tomato genes in protoplasts, linking editing efficiency to chromatin accessibility, genomic context, and sequence features. Open chromatin sites showed higher editing rates, while transcriptional activity had little effect, and a subset of guides produced near‑complete editing with microhomology‑mediated deletions. Human‑trained prediction models performed poorly, highlighting the need for plant‑specific guide design tools.

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 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.

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 integrates genome, transcriptome, and chromatin accessibility data from 380 soybean accessions to dissect the genetic and regulatory basis of symbiotic nitrogen fixation (SNF). Using GWAS, TWAS, eQTL mapping, and ATAC-seq, the authors identify key loci, co‑expression modules, and regulatory elements, and validate the circadian clock gene GmLHY1b as a negative regulator of nodulation via CRISPR and CUT&Tag. These resources illuminate SNF networks and provide a foundation for soybean improvement.

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.