Genetius

The study characterizes the plant spliceosomal protein AtSF1 in Arabidopsis thaliana, using iCLIP and RNA‑seq to map its in vivo branch point binding sites and demonstrate that loss of AtSF1 causes widespread 3' splice‑site mis‑selection. Structural comparison reveals a plant‑specific domain architecture, and the identified AtSF1 targets are enriched for circadian and defense genes, linking splicing regulation to timing and immunity.

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 identified two subclades of Arabidopsis NUDIX hydrolases that selectively hydrolyze distinct inositol pyrophosphate isomers, with subclade I targeting 4-InsP7 and subclade II targeting 3-InsP7 in a Mg2+-dependent manner. Loss-of-function mutants of subclade II NUDTs displayed disrupted phosphate and iron homeostasis, elevated 1/3-InsP7 levels, and increased resistance to Pseudomonas syringae, revealing roles in nutrient signaling and plant immunity, while cross-kingdom analyses showed conserved PP-InsP‑metabolizing activities.

The study demonstrates that a conserved clade of pentatricopeptide repeat (PPR) genes in Arabidopsis thaliana produces secondary siRNAs that enhance immunity against fungal and oomycete pathogens. These PPR loci, clustered on chromosome 1, have diversified through gene duplication, sequence variation, and pseudogenization, generating a heterogeneous siRNA pool likely involved in a co‑evolutionary arms race with pathogens. The authors define PPR‑derived siRNAs as a defense gene family with potential for engineering broad‑spectrum disease resistance.

The study used proximity labeling and other techniques to identify proteins that govern secretion of distinct extracellular vesicle (EV) subpopulations in Arabidopsis, revealing roles for EXO70 exocyst components, the immune protein RIN4, and VAP27 in EV biogenesis. Mutants in these pathways showed reduced EV release and heightened susceptibility to the fungal pathogen Colletotrichum higginsianum, highlighting EV secretion as a key factor in plant immunity.

The study examines the conservation and functional diversity of the EDVID motif within the coiled-coil domain of plant CC‑NLR immune receptors, integrating sequence analysis with structural data. It identifies the EDVID motif and a preceding acidic ‘preEDVID’ segment as predictors of canonical CC‑NLR activity, while also revealing a subset of CC‑NLRs that lack the motif and likely operate via an alternative mechanism.

The study identifies the RNA‑binding protein AtG3BP1 as a phosphorylation target of MAPKs MPK3, MPK4, and MPK6 at Ser257 in Arabidopsis thaliana and shows that this modification promotes susceptibility to bacterial pathogens, suppresses ROS accumulation and salicylic acid biosynthesis, and maintains stomatal opening. Phospho‑mimic and phospho‑dead mutants reveal that phosphorylation stabilizes AtG3BP1 by preventing proteasomal degradation, highlighting a novel post‑translational control layer in plant immunity.

The study reveals that Arabidopsis actin depolymerization factors (ADF2/3/4) have a nuclear moonlighting role, directly interacting with WRKY transcription factors to regulate immune‑related gene expression. Nuclear, rather than cytosolic, ADFs are essential for defense against both virulent and avirulent Pseudomonas syringae, highlighting a non‑canonical mechanism linking actin dynamics to transcriptional control in plant immunity.

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.