The study shows that the membrane lipids PI4P, PI(4,5)P2, and phosphatidylserine have distinct spatial and temporal dynamics during lateral root primordium formation in Arabidopsis thaliana, with PI4P acting as a stable basal lipid, PI(4,5)P2 serving as a negative regulator of initiation, and phosphatidylserine increasing after founder cell activation. Using live-cell biosensors, genetic mutants, and an inducible PI(4,5)P2 depletion system, the authors demonstrate that reducing PI(4,5)P2 enhances lateral root initiation and development.

The study engineers Type‑B response regulators to alter their transcriptional activity and cytokinin sensitivity, enabling precise modulation of cytokinin‑dependent traits. Using tissue‑specific promoters, the synthetic transcription factors were deployed in Arabidopsis thaliana to reliably increase or decrease lateral root numbers, demonstrating a modular platform for controlling developmental phenotypes.

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 characterizes the tomato class B heat shock factor SlHSFB3a, revealing its age‑dependent expression in roots and its role in enhancing lateral root density by modulating auxin homeostasis. Overexpression of SlHSFB3a increases lateral root emergence, while CRISPR‑mediated knockouts produce the opposite phenotype, indicating that SlHSFB3a regulates auxin signaling through repression of auxin repressors and activation of the ARF7/LOB20 pathway.

The study introduces a minimal precursor platform for synthetic trans-acting siRNAs (syn-tasiRNAs) in tomato, leveraging the endogenous SlmiR482b microRNA to produce functional silencing agents in both transgenic and virus-induced gene silencing (VIGS) systems. Minimal precursors successfully silenced endogenous genes and conferred resistance to tomato spotted wilt virus, and a transgene‑free delivery via crude extracts was demonstrated, highlighting a versatile tool for precision RNAi in Solanum lycopersicum.

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.