Genetius

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 identifies the cysteine‑rich receptor‑like kinase CRK5 as a negative regulator of salicylic‑acid‑mediated cell death and a positive regulator of antioxidant homeostasis during dark‑induced leaf senescence in Arabidopsis. Loss‑of‑function crk5 mutants display accelerated senescence, elevated ROS and electrolyte leakage, and altered antioxidant enzyme activities, phenotypes that are rescued by suppressing SA biosynthesis or catabolism. Transcriptome analysis reveals extensive deregulation of senescence‑ and redox‑related genes, highlighting CRK5’s central role in coordinating hormonal and oxidative pathways.

The study examined how elevated atmospheric CO₂ (550 ppm) affects immunity in the C₄ cereal maize (Zea mays L.) by exposing plants grown under ambient and elevated CO₂ to a range of pathogens. Elevated CO₂ increased susceptibility to sugarcane mosaic virus, decreased susceptibility to several bacterial and fungal pathogens, and left susceptibility to others unchanged, with reduced bacterial disease linked to heightened basal immune responses. These findings provide a baseline for future investigations into CO₂‑responsive defense mechanisms in C₄ crops.

The study shows that maize plants carrying autophagy-defective atg10 mutations exhibit delayed flowering and significant reductions in kernel size, weight, and number, culminating in lower grain yield. Reciprocal crossing experiments reveal that the maternal genotype, rather than the seed genotype, primarily drives the observed kernel defects, suggesting impaired nutrient remobilization from maternal tissues during seed development.

Using the bryophyte Physcomitrium patens, the study shows that loss of autophagy enhances auxin‑driven caulonemata differentiation and colony expansion under low nitrogen or imbalanced carbon/nitrogen conditions, accompanied by higher internal IAA, reduced PpPINA expression, and up‑regulated RSL transcription factors. Autophagy appears to suppress auxin‑induced differentiation during nutrient stress, acting as a hub that balances metabolic cues with hormonal signaling.

Thermopriming enhances heat stress tolerance by orchestrating protein maintenance pathways: it activates the heat shock response (HSR) via HSFA1 and the unfolded protein response (UPR) while modulating autophagy to clear damaged proteins. Unprimed seedlings cannot mount these responses, leading to proteostasis collapse, protein aggregation, and death, highlighting the primacy of HSR and protein maintenance over clearance mechanisms.

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 demonstrates that FERONIA and phytochrome B physically interact with the NADPH oxidase RBOHD, and that FERONIA-mediated phosphorylation of phyB is essential for RBOHD-driven ROS production under excess light stress in Arabidopsis thaliana. Additional membrane proteins CRK10 and PIP2;6 also associate with this complex, forming a plasma‑membrane assembly that integrates multiple signaling pathways to regulate stress‑induced ROS.

The study identifies wound‑induced proline transporters ProT2 and ProT3 as central regulators that link salicylic acid signaling to the suppression of de novo root regeneration (DNRR) via modulation of reactive oxygen species dynamics. Genetic loss of these transporters or pharmacological inhibition of proline transport alleviates SA‑mediated regeneration inhibition across several plant species without compromising disease resistance.

A genome-wide survey identified 217 EXO70 genes across five kiwifruit (Actinidia spp.) species, classifying them into three subfamilies and nine clades and revealing lineage‑specific expansions, especially in EXO70C, EXO70E, and EXO70H. Functional assays demonstrated that kiwifruit EXO70B1 interacts with the immune hub protein RIN4_1, suggesting a conserved EXO70‑RIN4 module in plant immunity. The study provides a foundational resource for exploring EXO70‑mediated disease resistance in kiwifruit.