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BTB-BACK Domain Protein POB1 Suppresses Immune Cell Death by Targeting Ubiquitin E3 ligase PUB17 for Degradation

Orosa, Beatriz; He, Qin; Mesmar, Joelle; Gilroy, Eleanor M.; McLellan, Hazel; Yang, Chengwei; Craig, Adam; Bailey, Mark; Zhang, Cunjin; Moore, Jonathan David; Boevink, Petra C.; Tian, Zhendong; Birch, Paul R.J.; Sadanandom, Ari

BTB-BACK Domain Protein POB1 Suppresses Immune Cell Death by Targeting Ubiquitin E3 ligase PUB17 for Degradation Thumbnail


Authors

Beatriz Orosa

Qin He

Joelle Mesmar

Eleanor M. Gilroy

Hazel McLellan

Chengwei Yang

Adam Craig

Mark Bailey

Jonathan David Moore

Petra C. Boevink

Zhendong Tian

Paul R.J. Birch



Abstract

Hypersensitive response programmed cell death (HR-PCD) is a critical feature in plant immunity required for pathogen restriction and prevention of disease development. The precise control of this process is paramount to cell survival and an effective immune response. The discovery of new components that function to suppress HR-PCD will be instrumental in understanding the regulation of this fundamental mechanism. Here we report the identification and characterisation of a BTB domain E3 ligase protein, POB1, that functions to suppress HR-PCD triggered by evolutionarily diverse pathogens. Nicotiana benthamiana and tobacco plants with reduced POB1 activity show accelerated HR-PCD whilst those with increased POB1 levels show attenuated HR-PCD. We demonstrate that POB1 dimerization and nuclear localization are vital for its function in HR-PCD suppression. Using protein-protein interaction assays, we identify the Plant U-Box E3 ligase PUB17, a well established positive regulator of plant innate immunity, as a target for POB1-mediated proteasomal degradation. Using confocal imaging and in planta immunoprecipitation assays we show that POB1 interacts with PUB17 in the nucleus and stimulates its degradation. Mutated versions of POB1 that show reduced interaction with PUB17 fail to suppress HR-PCD, indicating that POB1-mediated degradation of PUB17 U-box E3 ligase is an important step for negative regulation of specific immune pathways in plants. Our data reveals a new mechanism for BTB domain proteins in suppressing HR-PCD in plant innate immune responses.

Citation

Orosa, B., He, Q., Mesmar, J., Gilroy, E. M., McLellan, H., Yang, C., …Sadanandom, A. (2017). BTB-BACK Domain Protein POB1 Suppresses Immune Cell Death by Targeting Ubiquitin E3 ligase PUB17 for Degradation. PLoS Genetics, 13(1), Article e1006540. https://doi.org/10.1371/journal.pgen.1006540

Journal Article Type Article
Acceptance Date Dec 15, 2016
Online Publication Date Jan 5, 2017
Publication Date Jan 5, 2017
Deposit Date Jul 25, 2017
Publicly Available Date Mar 29, 2024
Journal PLoS Genetics
Print ISSN 1553-7390
Electronic ISSN 1553-7404
Publisher Public Library of Science
Peer Reviewed Peer Reviewed
Volume 13
Issue 1
Article Number e1006540
DOI https://doi.org/10.1371/journal.pgen.1006540

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Publisher Licence URL
http://creativecommons.org/licenses/by/4.0/

Copyright Statement
© 2017 Orosa et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.





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