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 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.