The Antagonist Function of <i>Arabidopsis</i> WRKY53 and ESR/ESP in Leaf Senescence Is Modulated by the Jasmonic and Salicylic Acid Equilibrium

Miao, Ying; Zentgraf, Ulrike

doi:10.1105/tpc.106.042705

Cited by 311 publications

(276 citation statements)

References 55 publications

(75 reference statements)

Supporting

Mentioning

263

Contrasting

Unclassified

Order By: Relevance

“…The Arabidopsis WRKY53 protein plays a regulatory role in the early events of leaf senescence (Miao et al, 2004). AtWRKY53 is a positive regulatory factor and regulates the expression of target genes directly, but an epithiospecifying senescence regulator (ESR) protein that is induced by jasmonic acid (JA) and inhibited by SA can block the process (Miao et al, 2007). AtWRKY70 participates in the regulation of leaf senescence as a negative regulatory factor, and delays the course of leaf senescence by restraining the expression of defense target genes regulated by SA, JA or ethylene (ET) (Ulker et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

WRKY22 Transcription Factor Mediates Dark-Induced Leaf Senescence in Arabidopsis

Zhou

Jiang

2011

Molecules and Cells

254

181

View full text Add to dashboard Cite

Arabidopsis WRKY proteins are plant-specific transcription factors, encoded by a large gene family, which contain the highly conserved amino acid sequence WRKYGQK and the zinc-finger-like motifs, Cys 2 His 2 or Cys 2 HisCys. They can recognize and bind the TTGAC(C/T) W-box ciselements found in the promoters of target genes, and are involved in the regulation of gene expression during pathogen defense, wounding, trichome development, and senescence. Here we investigated the physiological function of the Arabidopsis WRKY22 transcription factor during dark-induced senescence. WRKY22 transcription was suppressed by light and promoted by darkness. In addition, AtWRKY22 expression was markedly induced by H 2 O 2 . These results indicated that AtWRKY22 was involved in signal pathways in response to abiotic stress. Darktreated AtWRKY22 over-expression and knockout lines showed accelerated and delayed senescence phenotypes, respectively, and senescence-associated genes exhibited increased and decreased expression levels. Mutual regulation existed between AtWRKY22 and AtWRKY6, AtWR-KY53, and AtWRKY70, respectively. Moreover, AtWRKY22 could influence their relative expression levels by feedback regulation or by other, as yet unknown mechanisms in response to dark. These results prove that AtWRKY22 participates in the dark-induced senescence signal transduction pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

WRKY22 Transcription Factor Mediates Dark-Induced Leaf Senescence in Arabidopsis

Zhou

Jiang

2011

Molecules and Cells

254

181

View full text Add to dashboard Cite

show abstract

“…WRKY53 was first identified as a senescenceassociated gene and subsequently screened out as a member of the systemic acquired resistance signaling network (Hinderhofer and Zentgraf, 2001;Wang et al, 2006). This gene can interact with the jasmonic acid (JA)-inducible protein EPITHIOSPECIFYING SENESCENCE REGULATOR to mediate negative crosstalk between pathogen resistance and senescence (Miao and Zentgraf, 2007). Recent genetic analysis has suggested that WRKY53 positively regulates basal resistance by coordinating with WRKY70 and WRKY46 (Hu et al, 2012).…”

Section: Ngf Can Effectively Combine Gene Network and Expression Cuesmentioning

confidence: 99%

Revealing Shared and Distinct Gene Network Organization in Arabidopsis Immune Responses by Integrative Analysis

et al. 2015

View full text Add to dashboard Cite

Pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) are two main plant immune responses to counter pathogen invasion. Genome-wide gene network organizing principles leading to quantitative differences between PTI and ETI have remained elusive. We combined an advanced machine learning method and modular network analysis to systematically characterize the organizing principles of Arabidopsis (Arabidopsis thaliana) PTI and ETI at three network resolutions. At the single network node/ edge level, we ranked genes and gene interactions based on their ability to distinguish immune response from normal growth and successfully identified many immune-related genes associated with PTI and ETI. Topological analysis revealed that the top-ranked gene interactions tend to link network modules. At the subnetwork level, we identified a subnetwork shared by PTI and ETI encompassing 1,159 genes and 1,289 interactions. This subnetwork is enriched in interactions linking network modules and is also a hotspot of attack by pathogen effectors. The subnetwork likely represents a core component in the coordination of multiple biological processes to favor defense over development. Finally, we constructed modular network models for PTI and ETI to explain the quantitative differences in the global network architecture. Our results indicate that the defense modules in ETI are organized into relatively independent structures, explaining the robustness of ETI to genetic mutations and effector attacks. Taken together, the multiscale comparisons of PTI and ETI provide a systems biology perspective on plant immunity and emphasize coordination among network modules to establish a robust immune response.

show abstract

“…Furthermore, treatment of Arabidopsis leaves with the herbicide 3-aminotriazole inhibits catalase activity and causes hydrogen peroxide stress and increased expression of SAG genes . Next to that, the senescence-specific transcription factor WRKY53 is induced by hydrogen peroxide (Miao et al, 2004;Miao and Zentgraf, 2007). In general, it is believed that oxidative stress results in damage to the cell, which loses its viability, resulting in early ageing, as denoted by the free radical theory of ageing (Harman, 1956).…”

Section: Oxidative Stress and Early Ageing Of Old5mentioning

confidence: 99%

TheArabidopsis onset of leaf death5Mutation of Quinolinate Synthase Affects Nicotinamide Adenine Dinucleotide Biosynthesis and Causes Early Ageing

et al. 2008

View full text Add to dashboard Cite

Leaf senescence in Arabidopsis thaliana is a strict, genetically controlled nutrient recovery program, which typically progresses in an age-dependent manner. Leaves of the Arabidopsis onset of leaf death5 (old5) mutant exhibit early developmental senescence. Here, we show that OLD5 encodes quinolinate synthase (QS), a key enzyme in the de novo synthesis of NAD. The Arabidopsis QS was previously shown to carry a Cys desulfurase domain that stimulates reconstitution of the oxygen-sensitive Fe-S cluster that is required for QS activity. The old5 lesion in this enzyme does not affect QS activity but it decreases its Cys desulfurase activity and thereby the long-term catalytic competence of the enzyme. The old5 mutation causes increased NAD steady state levels that coincide with increased activity of enzymes in the NAD salvage pathway. NAD plays a key role in cellular redox reactions, including those of the tricarboxylic acid cycle. Broad-range metabolite profiling of the old5 mutant revealed that it contains higher levels of tricarboxylic acid cycle intermediates and nitrogen-containing amino acids. The mutant displays a higher respiration rate concomitant with increased expression of oxidative stress markers. We postulate that the alteration in the oxidative state is integrated into the plant developmental program, causing early ageing of the mutant.

show abstract

The Antagonist Function of Arabidopsis WRKY53 and ESR/ESP in Leaf Senescence Is Modulated by the Jasmonic and Salicylic Acid Equilibrium

Cited by 311 publications

References 55 publications

WRKY22 Transcription Factor Mediates Dark-Induced Leaf Senescence in Arabidopsis

WRKY22 Transcription Factor Mediates Dark-Induced Leaf Senescence in Arabidopsis

Revealing Shared and Distinct Gene Network Organization in Arabidopsis Immune Responses by Integrative Analysis

TheArabidopsis onset of leaf death5Mutation of Quinolinate Synthase Affects Nicotinamide Adenine Dinucleotide Biosynthesis and Causes Early Ageing

Contact Info

Product

Resources

About