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Protein phosphatase AP2C1 negatively regulates basal resistance and defense responses to Pseudomonas syringae.

ABSTRACT: Mitogen-activated protein kinases (MAPKs) mediate plant immune responses to pathogenic bacteria. However, less is known about the cell autonomous negative regulatory mechanism controlling basal plant immunity. We report the biological role of Arabidopsis thaliana MAPK phosphatase AP2C1 as a negative regulator of plant basal resistance and defense responses to Pseudomonas syringae. AP2C2, a closely related MAPK phosphatase, also negatively controls plant resistance. Loss of AP2C1 leads to enhanced pathogen-induced MAPK activities, increased callose deposition in response to pathogen-associated molecular patterns or to P. syringae pv. tomato (Pto) DC3000, and enhanced resistance to bacterial infection with Pto. We also reveal the impact of AP2C1 on the global transcriptional reprogramming of transcription factors during Pto infection. Importantly, ap2c1 plants show salicylic acid-independent transcriptional reprogramming of several defense genes and enhanced ethylene production in response to Pto. This study pinpoints the specificity of MAPK regulation by the different MAPK phosphatases AP2C1 and MKP1, which control the same MAPK substrates, nevertheless leading to different downstream events. We suggest that precise and specific control of defined MAPKs by MAPK phosphatases during plant challenge with pathogenic bacteria can strongly influence plant resistance.

SUBMITTER: Shubchynskyy V

PROVIDER: S-EPMC5444444 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature

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Protein phosphatase AP2C1 negatively regulates basal resistance and defense responses to Pseudomonas syringae.

Shubchynskyy Volodymyr V Boniecka Justyna J Schweighofer Alois A Simulis Justinas J Kvederaviciute Kotryna K Stumpe Michael M Mauch Felix F Balazadeh Salma S Mueller-Roeber Bernd B Boutrot Freddy F Zipfel Cyril C Meskiene Irute I

Journal of experimental botany 20170201 5

Mitogen-activated protein kinases (MAPKs) mediate plant immune responses to pathogenic bacteria. However, less is known about the cell autonomous negative regulatory mechanism controlling basal plant immunity. We report the biological role of Arabidopsis thaliana MAPK phosphatase AP2C1 as a negative regulator of plant basal resistance and defense responses to Pseudomonas syringae. AP2C2, a closely related MAPK phosphatase, also negatively controls plant resistance. Loss of AP2C1 leads to enhance ...[more]

PMID: 28062592

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Project description:The intrinsic defense mechanisms of plants toward pathogenic bacteria have been widely investigated for years and are still at the center of interest in plant biosciences research. This study investigated the role of the AtbZIP62 gene encoding a transcription factor (TF) in the basal defense and systemic acquired resistance in Arabidopsis using the reverse genetics approach. To achieve that, the atbzip62 mutant line (lacking the AtbZIP62 gene) was challenged with Pseudomonas syringae pv. tomato (Pst DC3000) inoculated by infiltration into Arabidopsis leaves at the rosette stage. The results indicated that atbzip62 plants showed an enhanced resistance phenotype toward Pst DC3000 vir over time compared to Col-0 and the susceptible disease controls, atgsnor1-3 and atsid2. In addition, the transcript accumulation of pathogenesis-related genes, AtPR1 and AtPR2, increased significantly in atbzip62 over time (0-72 h post-inoculation, hpi) compared to that of atgsnor1-3 and atsid2 (susceptible lines), with AtPR1 prevailing over AtPR2. When coupled with the recorded pathogen growth (expressed as a colony-forming unit, CFU mL-1), the induction of PR genes, associated with the salicylic acid (SA) defense signaling, in part explained the observed enhanced resistance of atbzip62 mutant plants in response to Pst DC3000 vir. Furthermore, when Pst DC3000 avrB was inoculated, the expression of AtPR1 was upregulated in the systemic leaves of Col-0, while that of AtPR2 remained at a basal level in Col-0. Moreover, the expression of AtAZI (a systemic acquired resistance -related) gene was significantly upregulated at all time points (0-24 h post-inoculation, hpi) in atbzip62 compared to Col-0 and atgsnor1-3 and atsid2. Under the same conditions, AtG3DPH exhibited a high transcript accumulation level 48 hpi in the atbzip62 background. Therefore, all data put together suggest that AtPR1 and AtPR2 coupled with AtAZI and AtG3DPH, with AtAZI prevailing over AtG3DPH, would contribute to the recorded enhanced resistance phenotype of the atbzip62 mutant line against Pst DC3000. Thus, the AtbZIP62 TF is proposed as a negative regulator of basal defense and systemic acquired resistance in plants under Pst DC3000 infection.

Project description:Plant-pathogen interactions involve sophisticated action and counteraction strategies from both parties. Plants can recognize pathogen derived molecules, such as conserved pathogen associated molecular patterns (PAMPs) and effector proteins, and subsequently activate PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI), respectively. However, pathogens can evade such recognitions and suppress host immunity with effectors, causing effector-triggered susceptibility (ETS). The differences among PTI, ETS, and ETI have not been completely understood. Toward a better understanding of PTI, ETS, and ETI, we systematically examined various defense-related phenotypes of Arabidopsis infected with different Pseudomonas syringae pv. maculicola ES4326 strains, using the virulence strain DG3 to induce ETS, the avirulence strain DG34 that expresses avrRpm1 (recognized by the resistance protein RPM1) to induce ETI, and HrcC(-) that lacks the type three secretion system to activate PTI. We found that plants infected with different strains displayed dynamic differences in the accumulation of the defense signaling molecule salicylic acid, expression of the defense marker gene PR1, cell death formation, and accumulation/localization of the reactive oxygen species, H2O2. The differences between PTI, ETS, and ETI are dependent on the doses of the strains used. These data support the quantitative nature of PTI, ETS, and ETI and they also reveal qualitative differences between PTI, ETS, and ETI. Interestingly, we observed the induction of large cells in the infected leaves, most obviously with HrcC(-) at later infection stages. The enlarged cells have increased DNA content, suggesting a possible activation of endoreplication. Consistent with strong induction of abnormal cell growth by HrcC(-), we found that the PTI elicitor flg22 also activates abnormal cell growth, depending on a functional flg22-receptor FLS2. Thus, our study has revealed a comprehensive picture of dynamic changes of defense phenotypes and cell fate determination during Arabidopsis-P. syringae interactions, contributing to a better understanding of plant defense mechanisms.

Dataset Information

Protein phosphatase AP2C1 negatively regulates basal resistance and defense responses to Pseudomonas syringae.

Publications

Protein phosphatase AP2C1 negatively regulates basal resistance and defense responses to Pseudomonas syringae.

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