Double-Stranded RNA-Binding Protein 4 Is Required for Resistance Signaling against Viral and Bacterial Pathogens

Shifeng Zhu; Rae Dong Jeong; Gah Hyun Lim; Keshun Yu; Caixia Wang; A. C. Chandra-Shekara; Duroy Navarre; Daniel F. Klessig; Aardra Kachroo; Pradeep Kachroo

doi:10.1016/j.celrep.2013.08.018

Double-Stranded RNA-Binding Protein 4 Is Required for Resistance Signaling against Viral and Bacterial Pathogens

Shifeng Zhu, Rae Dong Jeong, Gah Hyun Lim, Keshun Yu, Caixia Wang, A. C. Chandra-Shekara, Duroy Navarre, Daniel F. Klessig, Aardra Kachroo, Pradeep Kachroo

Plant Pathology

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

43 Scopus citations

Abstract

Plant viruses often encode suppressors of host RNA silencing machinery, which occasionally function as avirulence factors that are recognized by host resistance (R) proteins. For example, the Arabidopsis R protein, hypersensitive response to TCV (HRT), recognizes the turnip crinkle virus (TCV) coat protein (CP). HRT-mediated resistance requires the RNA-silencing component double-stranded RNA-binding protein 4 (DRB4) even though it neither is associated with the accumulation of TCV-specific small RNA nor requires the RNA silencing suppressor function of CP. HRT interacts with the cytosolic fraction of DRB4. Interestingly, TCV infection both increases the cytosolic DRB4 pool and inhibits the HRT-DRB4 interaction. The virulent R8A CP derivative, which induces a subset of HRT-derived responses, also disrupts this interaction. The differential localization of DRB4 in the presence of wild-type and R8A CP implies the importance of subcellular compartmentalization of DRB4. The requirement of DRB4 in resistance to bacterial infection suggests a universal role in R-mediated defense signaling

Original language	English
Pages (from-to)	1168-1184
Number of pages	17
Journal	Cell Reports
Volume	4
Issue number	6
DOIs	https://doi.org/10.1016/j.celrep.2013.08.018
State	Published - Sep 26 2013

Bibliographical note

Funding Information:
We are grateful to Guillaume Robin for help with the graphical abstract and slider image. We thank James Carrington for rdr and dcl mutants, Jeff Dangl for RPM1-MYC and RPS2-HA transgenic lines, Feng Qu for drb4 mutant and R8A, CPB, and CPC clones, Ken Shirasu for RAR1 antibodies, and Mark Farman for useful comments. We thank Joanne Holden for help with SA estimations, Qing-ming Gao for help with qRT-PCR, Ludmila Lapchyk for technical help, and Amy Crume for managing the plant growth facility. This work was supported by a grant from the National Science Foundation (IOS no. 10641576).

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology

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10.1016/j.celrep.2013.08.018

Cite this

@article{2db96725db8445ea8859f90119ccb566,

title = "Double-Stranded RNA-Binding Protein 4 Is Required for Resistance Signaling against Viral and Bacterial Pathogens",

abstract = "Plant viruses often encode suppressors of host RNA silencing machinery, which occasionally function as avirulence factors that are recognized by host resistance (R) proteins. For example, the Arabidopsis R protein, hypersensitive response to TCV (HRT), recognizes the turnip crinkle virus (TCV) coat protein (CP). HRT-mediated resistance requires the RNA-silencing component double-stranded RNA-binding protein 4 (DRB4) even though it neither is associated with the accumulation of TCV-specific small RNA nor requires the RNA silencing suppressor function of CP. HRT interacts with the cytosolic fraction of DRB4. Interestingly, TCV infection both increases the cytosolic DRB4 pool and inhibits the HRT-DRB4 interaction. The virulent R8A CP derivative, which induces a subset of HRT-derived responses, also disrupts this interaction. The differential localization of DRB4 in the presence of wild-type and R8A CP implies the importance of subcellular compartmentalization of DRB4. The requirement of DRB4 in resistance to bacterial infection suggests a universal role in R-mediated defense signaling",

author = "Shifeng Zhu and Jeong, {Rae Dong} and Lim, {Gah Hyun} and Keshun Yu and Caixia Wang and Chandra-Shekara, {A. C.} and Duroy Navarre and Klessig, {Daniel F.} and Aardra Kachroo and Pradeep Kachroo",

note = "Funding Information: We are grateful to Guillaume Robin for help with the graphical abstract and slider image. We thank James Carrington for rdr and dcl mutants, Jeff Dangl for RPM1-MYC and RPS2-HA transgenic lines, Feng Qu for drb4 mutant and R8A, CPB, and CPC clones, Ken Shirasu for RAR1 antibodies, and Mark Farman for useful comments. We thank Joanne Holden for help with SA estimations, Qing-ming Gao for help with qRT-PCR, Ludmila Lapchyk for technical help, and Amy Crume for managing the plant growth facility. This work was supported by a grant from the National Science Foundation (IOS no. 10641576). ",

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language = "English",

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AU - Zhu, Shifeng

AU - Jeong, Rae Dong

AU - Lim, Gah Hyun

AU - Yu, Keshun

AU - Wang, Caixia

AU - Chandra-Shekara, A. C.

AU - Navarre, Duroy

AU - Klessig, Daniel F.

AU - Kachroo, Aardra

AU - Kachroo, Pradeep

N1 - Funding Information: We are grateful to Guillaume Robin for help with the graphical abstract and slider image. We thank James Carrington for rdr and dcl mutants, Jeff Dangl for RPM1-MYC and RPS2-HA transgenic lines, Feng Qu for drb4 mutant and R8A, CPB, and CPC clones, Ken Shirasu for RAR1 antibodies, and Mark Farman for useful comments. We thank Joanne Holden for help with SA estimations, Qing-ming Gao for help with qRT-PCR, Ludmila Lapchyk for technical help, and Amy Crume for managing the plant growth facility. This work was supported by a grant from the National Science Foundation (IOS no. 10641576).

PY - 2013/9/26

Y1 - 2013/9/26

N2 - Plant viruses often encode suppressors of host RNA silencing machinery, which occasionally function as avirulence factors that are recognized by host resistance (R) proteins. For example, the Arabidopsis R protein, hypersensitive response to TCV (HRT), recognizes the turnip crinkle virus (TCV) coat protein (CP). HRT-mediated resistance requires the RNA-silencing component double-stranded RNA-binding protein 4 (DRB4) even though it neither is associated with the accumulation of TCV-specific small RNA nor requires the RNA silencing suppressor function of CP. HRT interacts with the cytosolic fraction of DRB4. Interestingly, TCV infection both increases the cytosolic DRB4 pool and inhibits the HRT-DRB4 interaction. The virulent R8A CP derivative, which induces a subset of HRT-derived responses, also disrupts this interaction. The differential localization of DRB4 in the presence of wild-type and R8A CP implies the importance of subcellular compartmentalization of DRB4. The requirement of DRB4 in resistance to bacterial infection suggests a universal role in R-mediated defense signaling

AB - Plant viruses often encode suppressors of host RNA silencing machinery, which occasionally function as avirulence factors that are recognized by host resistance (R) proteins. For example, the Arabidopsis R protein, hypersensitive response to TCV (HRT), recognizes the turnip crinkle virus (TCV) coat protein (CP). HRT-mediated resistance requires the RNA-silencing component double-stranded RNA-binding protein 4 (DRB4) even though it neither is associated with the accumulation of TCV-specific small RNA nor requires the RNA silencing suppressor function of CP. HRT interacts with the cytosolic fraction of DRB4. Interestingly, TCV infection both increases the cytosolic DRB4 pool and inhibits the HRT-DRB4 interaction. The virulent R8A CP derivative, which induces a subset of HRT-derived responses, also disrupts this interaction. The differential localization of DRB4 in the presence of wild-type and R8A CP implies the importance of subcellular compartmentalization of DRB4. The requirement of DRB4 in resistance to bacterial infection suggests a universal role in R-mediated defense signaling

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Double-Stranded RNA-Binding Protein 4 Is Required for Resistance Signaling against Viral and Bacterial Pathogens

Abstract

Bibliographical note

ASJC Scopus subject areas

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