Evidence map›Paper›PMID 31916083›Full record

ArticlePlant molecular biology2020

MKK4/MKK5-MPK1/MPK2 cascade mediates SA-activated leaf senescence via phosphorylation of NPR1 in Arabidopsis.

Jianjian Zhang, Jiong Gao, Zheng Zhu, Yi Song, Xiaoyan Wang, Xiaolei Wang, Xin Zhou

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Plant molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
8.1field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 49 citations in OpenAlex.

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  17. Sustained Incompatibility between MAPK Signaling and Pathogen Effectors.International journal of molecular sciences · 2020
    Review
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  19. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Jianjian ZhangState Key Laboratory of Genetic Engineering and Fudan Center for Genetic Diversity and Designing Agriculture, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Jiong GaoState Key Laboratory of Genetic Engineering and Fudan Center for Genetic Diversity and Designing Agriculture, School of Life Sciences, Fudan University, Shanghai, 200438, China. gaojiong001@163.com.
Zheng ZhuState Key Laboratory of Genetic Engineering and Fudan Center for Genetic Diversity and Designing Agriculture, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Yi SongState Key Laboratory of Genetic Engineering and Fudan Center for Genetic Diversity and Designing Agriculture, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Xiaoyan WangState Key Laboratory of Genetic Engineering and Fudan Center for Genetic Diversity and Designing Agriculture, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Xiaolei WangState Key Laboratory of Genetic Engineering and Fudan Center for Genetic Diversity and Designing Agriculture, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Xin ZhouState Key Laboratory of Genetic Engineering and Fudan Center for Genetic Diversity and Designing Agriculture, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Fudan University · CN

Funding

Science and Technology Commission of Shanghai Municipality 2015JC1400800the National Natural Science Foundation of China 31700246
6 · The paper itself

Abstract

The mechanism by which endogenous salicylic acid (SA) regulates leaf senescence remains elusive. Here we provide direct evidence that an enhancement of endogenous SA level, via chemical-induced upregulation of ISOCHORISMATE SYNTHASE 1 (ICS1), could significantly accelerate the senescence process of old leaves through mediation of the key SA signaling component NON EXPRESSOR OF PATHOGENESIS RELATED GENES 1 (NPR1) in Arabidopsis. Importantly, by taking advantage of this chemically induced leaf senescence system, we identified a mitogen-activated protein kinase (MAPK) cascade MKK4/5-MPK1/2 that is required for the SA/NPR1-mediated leaf senescence. Both MKK4/5 and MPK1/2 exhibited SA-induced kinase activities, with MPK1/2 being the immediate targets of MKK4/5. Double mutants of mkk4 mkk5 and mpk1 mpk2 displayed delayed leaf senescence, while constitutive overexpression of the kinase genes led to premature leaf senescence. Such premature leaf senescence was suppressed when they were overexpressed in an SA synthesis defective mutant (sid2) or signaling detective mutant (npr1). We further showed that MPK1, but not MPK2, could directly phosphorylate NPR1. Meanwhile, MPK1 also mediated NPR1 monomerization. Notably, induction of disease resistance was significantly compromised in the single and double mutants of the kinase genes. Taken together, our data demonstrate that the MKK4/5-MPK1/2 cascade plays a critical role in modulating SA signaling through a complex regulatory network in Arabidopsis.

Indexed as

Gene Expression Regulation, PlantMAP Kinase Signaling SystemArabidopsisArabidopsis ProteinsMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesPhosphorylationPlant LeavesPlants, Genetically ModifiedSalicylic AcidSignal TransductionArabidopsis ProteinsATMPK1 protein, ArabidopsisMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesMKK4 protein, ArabidopsisMKK5 protein, ArabidopsisMPK2 protein, ArabidopsisNPR1 protein, ArabidopsisSalicylic AcidMAPKsNPR1ProbenazoleSA

Identifiers

PMID31916083
OpenAlexW3000432743

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.