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 created a system that blocks root‑mediated signaling between wheat varieties in a varietal mixture and used transcriptomic and metabolomic profiling to reveal that root chemical interactions drive reduced susceptibility to Septoria tritici blotch, with phenolic compounds emerging as key mediators. Disruption of these root signals eliminates both the disease resistance phenotype and the associated molecular 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 characterizes the chloroplast‑localized protein AT4G33780 in Arabidopsis thaliana using CRISPR/Cas9 knockout and overexpression lines, revealing tissue‑specific expression and context‑dependent effects on seed germination, seedling growth, vegetative development, and root responses to nickel stress. Integrated transcriptomic (RNA‑seq) and untargeted metabolomic analyses show extensive transcriptional reprogramming—especially of cell‑wall genes—and altered central energy metabolism, indicating AT4G33780 coordinates metabolic state with developmental regulation rather than controlling single 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 establishes a tractable system using the large bloom-forming diatom Coscinodiscus granii and its natural oomycete parasite Lagenisma coscinodisci, enabling manual isolation of single host cells and stable co-cultures. High‑quality transcriptomes for both partners were assembled, revealing diverse oomycete effectors and a host transcriptional response involving proteases and exosome pathways, while also profiling the co‑occurring heterotrophic flagellate Pteridomonas sp. This tripartite platform provides a unique marine model for dissecting molecular mechanisms of oomycete‑diatom interactions.