Pseudomonas syringae Type III Effector HopBB1 Promotes Host Transcriptional Repressor Degradation to Regulate Phytohormone Responses and Virulence
| Autor: | Omri M. Finkel, Jeffery L. Dangl, Petra Epple, Yijian He, Paulo José Pereira Lima Teixeira, Surojit Biswas, Marie E. English, Li Yang, Piotr A. Mieczkowski, Isai Salas-González |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Arabidopsis Pseudomonas syringae Virulence Repressor Cyclopentanes Microbiology Article 03 medical and health sciences chemistry.chemical_compound Bacterial Proteins Plant Growth Regulators Gene Expression Regulation Plant Virology Tobacco Plant Immunity Oxylipins Promoter Regions Genetic Transcription factor Plant Diseases Genetics biology Arabidopsis Proteins Basic Helix-Loop-Helix Leucine Zipper Transcription Factors Effector Jasmonic acid biology.organism_classification Repressor Proteins 030104 developmental biology Regulon chemistry Host-Pathogen Interactions Parasitology Signal Transduction Transcription Factors |
| Zdroj: | Cell Host & Microbe. 21:156-168 |
| ISSN: | 1931-3128 |
| Popis: | Independently evolved pathogen effectors from three branches of life (ascomycete, eubacteria and oomycete) converge onto the Arabidopsis TCP14 transcription factor to manipulate host defense. However, the mechanistic basis for defense control via TCP14 regulation is unknown. We demonstrate that TCP14 regulates the plant immune system by transcriptionally repressing a subset of the Jasmonic acid (JA) hormone signaling outputs. A previously unstudied Pseudomonas syringae (Psy) type III effector, HopBB1, interacts with TCP14 and targets it to the SCFCOI1- degradation complex by connecting it to the JA signaling repressor JAZ3. Consequently, HopBB1 de-represses the TCP14-regulated subset of JA response genes and promotes pathogen virulence. Thus, HopBB1 fine-tunes host phytohormone crosstalk by precisely manipulating part of the JA regulon to avoid pleiotropic host responses, while promoting pathogen proliferation. |
| Databáze: | OpenAIRE |
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