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 identified a heat‑responsive exon‑skipping event in the basic Helix‑Loop‑Helix domain of the transcription factor PIF4, which reduces PIF4 activity and promotes photomorphogenic traits in etiolated seedlings. This reveals a novel post‑transcriptional mechanism by which plants modulate PIF4 function during heat stress.
The authors used a bottom‑up thermodynamic modelling framework to investigate how plants decode calcium signals, starting from Ca2+ binding to EF‑hand proteins and extending to higher‑order decoding modules. They identified six universal Ca2+-decoding modules that can explain variations in calcium sensitivity among kinases and provide a theoretical basis for interpreting calcium signal amplitude and frequency in plant cells.
The study identifies two diel regulatory modules that coordinate plant cuticle formation: the LRB‑phyB‑PIF4 pathway suppresses wax biosynthesis during daylight, while the COP1‑CFLAP1 pathway promotes cutin accumulation at night. Degradation of phyB and CFLAP1 via specific E3 ubiquitin ligases modulates the activity of transcription factors PIF4 and BDG1 to ensure timely cuticle assembly.
The study shows that high ambient temperature triggers extensive changes in ROS homeostasis in Arabidopsis seedlings, with H2O2 balance being essential for thermomorphogenic hypocotyl elongation. PIF4 directly activates catalase genes CAT2 and CAT3 to regulate H2O2 levels, forming a PIF4‑CAT‑H2O2 module that operates alongside the PIF4‑auxin pathway, while elevated H2O2 feeds back to reduce PIF4 protein abundance.
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.
The study demonstrates that the microtubule‑associated protein WDL4 is essential for PhyB‑dependent thermomorphogenic and photomorphogenic responses in Arabidopsis, as wdl4-3 mutants mimic phyB loss‑of‑function phenotypes under varying temperatures and light conditions. Genetic analyses reveal that PIF4 activity is required for wdl4-3 hypocotyl hyper‑elongation, and while exogenous auxin can rescue pif4‑related defects, it does not restore the wdl4-3 specific elongation, indicating additional regulatory layers.