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.
Clathrin-coated vesicles are targeted for selective autophagy during osmotic stress.
Authors: dragwidge, j., Buridan, M., Kraus, J., Kosuth, T., Chambaud, C., Brocard, L., Yperman, K., Mylle, E., Vandorpe, M., Eeckhout, D., De Jaeger, G., Pleskot, R., Bernard, A., Van Damme, D.
The study identifies an autophagy pathway that degrades plasma membrane-derived clathrin-coated vesicles (CCVs) during hyperosmotic stress, helping maintain membrane tension as cell volume decreases. Using live imaging and correlative microscopy, the authors show that the TPLATE complex subunits AtEH1/Pan1 and AtEH2/Pan1 act as selective autophagy receptors by directly binding ATG8, thereby removing excess membrane under drought or salt conditions.
The study presents an optimized Agrobacterium-mediated transformation protocol for bread wheat that incorporates a GRF4‑GIF1 fusion to enhance regeneration and achieve genotype‑independent transformation across multiple cultivars. The approach consistently improves transformation efficiency while limiting pleiotropic effects, offering a versatile platform for functional genomics and gene editing in wheat.
The study examines how the SnRK1 catalytic subunit KIN10 integrates carbon availability with root growth regulation in Arabidopsis thaliana. Loss of KIN10 reduces glucose‑induced inhibition of root elongation and triggers widespread transcriptional reprogramming of metabolic and hormonal pathways, notably affecting auxin and jasmonate signaling under sucrose supplementation. These findings highlight KIN10 as a central hub linking energy status to developmental and environmental cues in roots.