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.
Arabidopsis lines with modified ascorbate concentrations reveal a link between ascorbate and auxin biosynthesis
Authors: Fenech, M., Zulian, V., Moya-Cuevas, J., Arnaud, D., Morilla, I., Smirnoff, N., Botella, M. A., Stepanova, A. N., Alonso, J. M., Martin-Pizarro, C., Amorim-Silva, V.
The study used Arabidopsis thaliana mutants with low (vtc2, vtc4) and high (vtc2/OE-VTC2) ascorbate levels to examine how ascorbate concentration affects gene expression and cellular homeostasis. Transcriptomic analysis revealed that altered ascorbate levels modulate defense and stress pathways, and that TAA1/TAR2‑mediated auxin biosynthesis is required for coping with elevated ascorbate in a light‑dependent manner.
The study employed a multi‑omics workflow (transcriptomics, ribosome profiling, and proteomics) to uncover small peptides encoded by long non‑coding RNAs (LSEPs) in rice, finding that over 40% of surveyed lncRNAs associate with ribosomes. An optimized small‑peptide extraction followed by LC‑MS/MS identified 403 LSEPs, confirming the peptide‑coding capacity of plant lncRNAs and providing a scalable pipeline for large‑scale screening.
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.
A biparental Vicia faba mapping population was screened under glasshouse conditions for resistance to a mixture of Fusarium avenaceum and Fusarium oxysporum, revealing several families with moderate to high resistance. Using the Vfaba_v2 Axiom SNP array, a high-density linkage map of 6,755 SNPs was constructed, enabling the identification of a major QTL on linkage group 4 associated with partial resistance to foot and root rot.
The study shows that silencing of NOR2 rRNA genes in Arabidopsis thaliana depends primarily on CHH-context cytosine methylation, particularly mediated by CMT2 and the chromatin remodeler DDM1, rather than CG or CHG methylation. Comparative promoter analysis revealed a prevalence of CHH sites in plant rDNA promoters, explaining why CHH methylation mutants disrupt NOR2 silencing more strongly, while NOR2 loci are hyper‑methylated and more condensed than NOR4.