Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 42383854

The bZIP54 (GBF2)-SARD1 module regulates salicylic acid-mediated resistance to Pst DC3000 in Arabidopsis.

Charles Tetteh·Cheng Zhang·Sheng Luo·Yanyan Wang·Ting Zhang·Pinyuan Jin·Yawen Liang·Yiling Wang·Chenxi Liu·Huajian Zhang
View original source ↗Export metadata ↓

Abstract

Salicylic acid (SA)-mediated defense responses are crucial for plant immunity, yet transcription factors (TFs) that coordinate SA biosynthesis with immune activation remain incompletely characterized. Here, a basic leucine zipper (bZIP) TF, bZIP54, was identified as a positive regulator in response to Pseudomonas syringae pv. tomato (Pst) DC3000. Consistent with this finding, bZIP54 regulated SA accumulation and a suite of SA-related defense genes following Pst DC3000 infection. Mechanistically, bZIP54 directly bound to a G-box-like motif in the SARD1 promoter, activating its expression-an interaction that was further enhanced by SA. Genetic analysis demonstrated that SARD1 operates downstream of bZIP54 to confer resistance to Pst DC3000. Additionally, bZIP54 also contributed to defense against the fungal pathogen Sclerotinia sclerotiorum, indicating a broader role in plant immunity. Together, these findings revealed a bZIP54-SARD1 regulatory module, thus providing insights into the transcriptional networks governing disease resistance in Arabidopsis.

Explore related subjects

ArabidopsisSalicylic AcidPseudomonas syringaeArabidopsis ProteinsPlant DiseasesGene Expression Regulation, PlantBasic-Leucine Zipper Transcription FactorsDisease ResistanceAscomycotaPromoter Regions, GeneticPlant ImmunityPlants, Genetically ModifiedJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Charles Tetteh, Cheng Zhang, Sheng Luo, Yanyan Wang, Ting Zhang, Pinyuan Jin, Yawen Liang, Yiling Wang, Chenxi Liu, Huajian Zhang. 2026-09-01. The bZIP54 (GBF2)-SARD1 module regulates salicylic acid-mediated resistance to Pst DC3000 in Arabidopsis.. https://doi.org/10.1093/plphys%2Fkiag420

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2026

Dual regulation of the receptor-like kinase BIR1 involves site-directed transcript cleavage and 5'-leader-mediated translational control.

In Arabidopsis, BRASSINOSTEROID INSENSITIVE1-ASSOCIATED RECEPTOR KINASE 1 (BAK1)-INTERACTING RECEPTOR-LIKE KINASE 1 (BIR1) is a negative regulator of plant immunity and cell death. BIR1 was earlier described as a target of epigenetic and post-transcriptional degradation. During virus infections, degradome analysis of BIR1 transcripts mapped predominant mRNA cleavage sites at the 5'-untranslated leader region (site A) and the protein-coding sequence (sites B and C). Here, we identified another virus-associated cleavage site (D) within the BIR1 coding region and investigated the contribution of site-directed mRNA cleavage to BIR1 regulation. Mutations at B, C, and D sites enhanced mRNA stability by impairing transcript cleavage, resulting in increased BIR1 mRNA and protein accumulation. This regulation is disrupted in RNA silencing mutants, supporting a model of cis-directed small interfering RNA (siRNA)-mediated degradation. We next demonstrate that virus infection reduces BIR1 translation in Arabidopsis. Furthermore, our data reveal a repressive role for the 5'-leader in regulating BIR1 translation, potentially mediated by upstream open reading frames (uORFs) and a virus-responsive long non-coding RNA (lncRNA) derived from the natural antisense At4g39838 locus. Together, these findings reveal a multilayered regulatory mechanism that integrates sRNA-mediated cleavage with translational control, with broader implications for the fine-tuning of stress-responsive gene expression during infection.

Arabidopsis↗
PubMed2026

The genetic control of rapid genome content divergence in Arabidopsis thaliana.

Genome evolution in eukaryotes is predominantly driven by the dynamics of repetitive sequences, which vary widely in both copy number and sequence composition. Rates of repeat evolution differ between and within species and are likely modulated by both genetics and environment. To uncover factors shaping the rate of genome content evolution, we analyzed 1043 resequenced Arabidopsis thaliana genomes using a novel K-mer-based approach to characterize genome content variation and identify hypervariable regions underlying differences in repeat abundance. We next treated repeat abundance as a quantitative trait and performed genome-wide association analyses across more than 400 repeat families to identify the genetic basis of copy number variation. Integrating these results through a meta-GWAS approach revealed both cis-acting variants and more than 50 candidate trans-acting loci associated with repeat abundance genome-wide. Cis-acting variation was predominantly localized to pericentromeric and centromeric regions, whereas trans-acting loci were enriched for candidate genes involved in DNA replication, DNA repair, and DNA methylation regulation. The results are consistent with purifying selection acting against mutations that accelerate genome content divergence, favoring alleles that constrain repeat expansion. Together, these findings provide new insights into the genetic architecture and evolutionary forces shaping genome evolution in A. thaliana and establish a framework for investigating these processes in other plant species.

Arabidopsis↗
PubMed2026

ARR1 and ARR12 negatively regulate arsenic stress tolerance by controlling flavonoid metabolism in Arabidopsis.

ARR1/12-mediated cytokinin signaling negatively regulates the accumulation of glycosylated flavonoids, thereby increasing plant susceptibility to As(III) stress. Cytokinins negatively regulate arsenic stress tolerance in plants through cytokinin-signaling type-B Arabidopsis response regulators (B-ARRs), specifically ARR1 and ARR12. However, the mechanism by which cytokinin signaling regulates plant metabolite dynamics, particularly antioxidant flavonoids, in response to arsenic toxicity remains largely unknown. Here, we hypothesized that ARR1/12-mediated cytokinin signaling modulates flavonoid metabolism to regulate arsenite [As(III)] tolerance. By comparing the global metabolic changes in roots of the arr1 12 double mutant (rD) and wild-type (WT) plants, we found that As(III) stress globally reduced metabolite abundance in WT roots. Importantly, the rD mutant accumulated significantly more flavonoids, most in glycosylated forms, than WT under As(III) exposure, which was supported by the specific upregulation of UDP-glycosyltransferase genes involved in flavonoid glycosylation. Accordingly, exogenous application of the glycosylated quercitrin-enhanced As(III) tolerance in WT roots, strengthening that the increase of glycosylated flavonoids in rD roots was beneficial for plant survival under As(III) exposure. Our data collectively strongly support that the increased glycosylation of flavonoids in the rD mutant improves their antioxidant functionality, thereby enhancing the As(III) stress tolerance. This study provides a new insight into the negative role of cytokinin signaling in repressing glycosylated flavonoid accumulation, causing increased susceptibility of plants to As(III) stress. Manipulation of cytokinin signaling or flavonoid glycosylation is, therefore, a promising approach for heavy metal stress mitigation in crops.

Arabidopsis↗