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.

Using hydathode-focused inoculation, the study mapped a major QTL on Arabidopsis chromosome 5 and identified the CNL-type immune receptor SUT1 as a novel resistance gene that restricts early colonization of Xanthomonas campestris pv. campestris in hydathodes. Functional analyses showed SUT1 acts independently of the known RKS1/ZAR1 complex and provides tissue‑specific resistance, being effective primarily in hydathodes but not in xylem.

A biparental Vicia faba mapping population was screened under glasshouse conditions for resistance to a mixture of Fusarium avenaceum and Fusarium oxysporum, revealing several families with moderate to high resistance. Using the Vfaba_v2 Axiom SNP array, a high-density linkage map of 6,755 SNPs was constructed, enabling the identification of a major QTL on linkage group 4 associated with partial resistance to foot and root rot.

The study investigated unexpected leaf spot symptoms in Psa3‑resistant kiwifruit (Actinidia) germplasm, finding that Psa3 was detectable by qPCR and metabarcoding despite poor culturing. Metabarcoding revealed distinct bacterial community shifts in lesions versus healthy tissue, and whole‑genome sequencing identified diverse Pseudomonas spp. that, while not individually more pathogenic, could enhance Psa3 growth, suggesting pathogenic consortia on resistant hosts.