Pseudomonas syringae Type III Effector HopBB1 Promotes Host Transcriptional Repressor Degradation to Regulate Phytohormone Responses and Virulence

Li Yang; Paulo José Pereira Lima Teixeira; Surojit Biswas; Omri M. Finkel; Yijian He; Isai Salas-Gonzalez; Marie E. English; Petra Epple; Piotr Mieczkowski; Jeffery L. Dangl

doi:10.1016/j.chom.2017.01.003

Pseudomonas syringae Type III Effector HopBB1 Promotes Host Transcriptional Repressor Degradation to Regulate Phytohormone Responses and Virulence

Li Yang, Paulo José Pereira Lima Teixeira, Surojit Biswas, Omri M. Finkel, Yijian He, Isai Salas-Gonzalez, Marie E. English, Petra Epple, Piotr Mieczkowski, Jeffery L. Dangl^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

100 Scopus citations

Abstract

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 SCF^COI1 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.

Original language	English
Pages (from-to)	156-168
Number of pages	13
Journal	Cell Host and Microbe
Volume	21
Issue number	2
DOIs	https://doi.org/10.1016/j.chom.2017.01.003
State	Published - 8 Feb 2017
Externally published	Yes

Bibliographical note

Publisher Copyright:
© 2017 Elsevier Inc.

Keywords

HopBB1
JAZ
Pseudomonas syringae
RNA-seq
TCP
hormone crosstalk
jasmonic acid
plant immunity
sub-nuclear foci
virulence effector

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10.1016/j.chom.2017.01.003

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Yang, L., Teixeira, P. J. P. L., Biswas, S., Finkel, O. M., He, Y., Salas-Gonzalez, I., English, M. E., Epple, P., Mieczkowski, P., & Dangl, J. L. (2017). Pseudomonas syringae Type III Effector HopBB1 Promotes Host Transcriptional Repressor Degradation to Regulate Phytohormone Responses and Virulence. Cell Host and Microbe, 21(2), 156-168. https://doi.org/10.1016/j.chom.2017.01.003

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title = "Pseudomonas syringae Type III Effector HopBB1 Promotes Host Transcriptional Repressor Degradation to Regulate Phytohormone Responses and Virulence",

abstract = "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.",

keywords = "HopBB1, JAZ, Pseudomonas syringae, RNA-seq, TCP, hormone crosstalk, jasmonic acid, plant immunity, sub-nuclear foci, virulence effector",

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Yang, L, Teixeira, PJPL, Biswas, S, Finkel, OM, He, Y, Salas-Gonzalez, I, English, ME, Epple, P, Mieczkowski, P & Dangl, JL 2017, 'Pseudomonas syringae Type III Effector HopBB1 Promotes Host Transcriptional Repressor Degradation to Regulate Phytohormone Responses and Virulence', Cell Host and Microbe, vol. 21, no. 2, pp. 156-168. https://doi.org/10.1016/j.chom.2017.01.003

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AU - Yang, Li

AU - Teixeira, Paulo José Pereira Lima

AU - Biswas, Surojit

AU - Finkel, Omri M.

AU - He, Yijian

AU - Salas-Gonzalez, Isai

AU - English, Marie E.

AU - Epple, Petra

AU - Mieczkowski, Piotr

AU - Dangl, Jeffery L.

PY - 2017/2/8

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N2 - 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.

AB - 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.

KW - HopBB1

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KW - hormone crosstalk

KW - jasmonic acid

KW - plant immunity

KW - sub-nuclear foci

KW - virulence effector

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Pseudomonas syringae Type III Effector HopBB1 Promotes Host Transcriptional Repressor Degradation to Regulate Phytohormone Responses and Virulence

Abstract

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Keywords

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