The study characterizes a conserved RNA structural element named DEAD within DEAD-box helicase genes in land plants, showing that it functions as a sensor of helicase activity to regulate alternative splicing in Arabidopsis thaliana. By modulating the folding of DEAD, the plant balances helicase transcript and protein levels via a negative feedback loop, and loss of this regulation leads to widespread splicing disruptions and severe stress phenotypes.

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 demonstrates that the plastid chaperone CLPC2, but not its paralogue CLPC1, is essential for Arabidopsis responsiveness to microbial volatile compounds and for normal seed and seedling development. Loss of CLPC2 alters the chloroplast proteome, affecting proteins linked to growth, photosynthesis, and embryogenesis, while overexpression of CLPC2 mimics CLPC1 deficiency, highlighting distinct functional roles within the CLP protease complex.

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.