The study examined electrophysiological responses of young poplar trees to controlled stem bending and root pressurization, identifying a distinct gradual potential (GP) whose amplitude and propagation are modulated by stimulus speed and intensity. Results indicate that mechanical stress generates a transient hydraulic pressure wave that triggers the GP, suggesting a hydraulic‑electrical coupling mechanism that encodes detailed mechanical information for adaptive responses to wind.

The study used CRISPR/Cas9 to generate rice snrk1 mutants and performed integrated phenotypic, transcriptomic, proteomic, and phosphoproteomic analyses under normal and starvation conditions, revealing SnRK1’s dual role in promoting growth and mediating stress responses. Findings indicate sub-functionalization of SnRK1 subunits and identify novel phosphorylation targets linked to membrane trafficking, ethylene signaling, and ion transport.

The study profiled root transcriptomes of Arabidopsis wild type and etr1 gain-of-function (etr1-3) and loss-of-function (etr1-7) mutants under ethylene or ACC treatment, identifying 4,522 ethylene‑responsive transcripts, including 553 that depend on ETR1 activity. ETR1‑dependent genes encompassed ethylene biosynthesis enzymes (ACO2, ACO3) and transcription factors, whose expression was further examined in an ein3eil1 background, revealing that both ETR1 and EIN3/EIL1 pathways regulate parts of the network controlling root hair proliferation and lateral root formation.

The study reveals that the plant immune regulator NPR1 is modulated by opposing post‑translational modifications mediated by the nutrient‑sensing kinases TOR and SnRK1. Under normal conditions TOR phosphorylates NPR1 at Ser‑55/59 to suppress its activity, while salicylic‑acid‑induced SnRK1 activation inhibits TOR and phosphorylates NPR1 at Ser‑557, thereby activating NPR1 and linking metabolic status to immune signaling.

The study shows that the SnRK1 catalytic subunit KIN10 directs tissue-specific growth‑defense programs in Arabidopsis thaliana by reshaping transcriptomes. kin10 knockout mutants exhibit altered root transcription, reduced root growth, and weakened defense against Pseudomonas syringae, whereas KIN10 overexpression activates shoot defense pathways, increasing ROS and salicylic acid signaling at the cost of growth.

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 examined early metabolic responses to salt stress in a salt‑tolerant alfalfa cultivar, focusing on SnRK1 activity, sucrose, and trehalose‑6‑phosphate dynamics during leaf expansion. Hydroponically grown plants exposed to 200 mM NaCl showed rapid, wave‑like SnRK1 activation within 1 hour, a transient decline in chloroplast performance, and an uncoupling of the Tre6P‑sucrose regulatory link, with a second SnRK1 peak correlating with reduced leaf growth. Exogenous sucrose inhibited SnRK1 activity, highlighting early SnRK1 activation as a pivotal component of salt stress adaptation.

The study investigated how Arabidopsis thaliana SR protein kinases (AtSRPKs) regulate alternative RNA splicing by using chemical inhibitors of SRPK activity. Inhibition with SPHINX31 and SRPIN340 caused reduced root growth and loss of root hairs, accompanied by widespread changes in splicing and phosphorylation of genes linked to root development and other cellular processes. Multi‑omics analysis (transcriptomics and phosphoproteomics) revealed that AtSRPKs modulate diverse splicing factors and affect the splicing landscape of numerous pathways.

The study investigates the role of the Arabidopsis transcription factor AtMYB93 in sulfur (S) signaling and root development, revealing that AtMYB93 mutants exhibit altered expression of S transport and metabolism genes and increased shoot S levels, while tomato plants overexpressing SlMYB93 show reduced shoot S. Transcriptomic profiling, elemental analysis, and promoter activity assays indicate that AtMYB93 contributes to root responses to S deprivation, though functional redundancy masks clear phenotypic effects on lateral and adventitious root formation.

The study investigates the Arabidopsis ribosomal protein RPS6A and its role in auxin‑related root growth, revealing that rps6a mutants display shortened primary roots, fewer lateral roots, and defective vasculature that are not rescued by exogenous auxin. Cell biological observations and global transcriptome profiling show weakened auxin signaling and reduced levels of PIN auxin transporters in the mutant, indicating a non‑canonical function of the ribosomal subunit in auxin pathways.