Imperial College London

Dr Tolga Bozkurt

Faculty of Natural SciencesDepartment of Life Sciences

Reader in Molecular Plant-Microbe
 
 
 
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Contact

 

+44 (0)20 7594 5381o.bozkurt

 
 
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Location

 

6167Sir Alexander Fleming BuildingSouth Kensington Campus

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Summary

 

Publications

Citation

BibTex format

@article{Gao:2020:10.1073/pnas.2002759117,
author = {Gao, C and Xu, H and Huang, J and Sun, B and Zhang, F and Savage, Z and Duggan, C and Yan, T and Wu, C-H and Wang, Y and Vleeshouwers, VGAA and Kamoun, S and Bozkurt, TO and Dong, S},
doi = {10.1073/pnas.2002759117},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
pages = {9613--9620},
title = {Pathogen manipulation of chloroplast function triggers a light-dependent immune recognition},
url = {http://dx.doi.org/10.1073/pnas.2002759117},
volume = {117},
year = {2020}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - In plants and animals, nucleotide-binding leucine-rich repeat (NLR) proteins are intracellular immune sensors that recognize and eliminate a wide range of invading pathogens. NLR-mediated immunity is known to be modulated by environmental factors. However, how pathogen recognition by NLRs is influenced by environmental factors such as light remains unclear. Here, we show that the agronomically important NLR Rpi-vnt1.1 requires light to confer disease resistance against races of the Irish potato famine pathogen Phytophthora infestans that secrete the effector protein AVRvnt1. The activation of Rpi-vnt1.1 requires a nuclear-encoded chloroplast protein, glycerate 3-kinase (GLYK), implicated in energy production. The pathogen effector AVRvnt1 binds the full-length chloroplast-targeted GLYK isoform leading to activation of Rpi-vnt1.1. In the dark, Rpi-vnt1.1–mediated resistance is compromised because plants produce a shorter GLYK—lacking the intact chloroplast transit peptide—that is not bound by AVRvnt1. The transition between full-length and shorter plant GLYK transcripts is controlled by a light-dependent alternative promoter selection mechanism. In plants that lack Rpi-vnt1.1, the presence of AVRvnt1 reduces GLYK accumulation in chloroplasts counteracting GLYK contribution to basal immunity. Our findings revealed that pathogen manipulation of chloroplast functions has resulted in a light-dependent immune response.
AU - Gao,C
AU - Xu,H
AU - Huang,J
AU - Sun,B
AU - Zhang,F
AU - Savage,Z
AU - Duggan,C
AU - Yan,T
AU - Wu,C-H
AU - Wang,Y
AU - Vleeshouwers,VGAA
AU - Kamoun,S
AU - Bozkurt,TO
AU - Dong,S
DO - 10.1073/pnas.2002759117
EP - 9620
PY - 2020///
SN - 0027-8424
SP - 9613
TI - Pathogen manipulation of chloroplast function triggers a light-dependent immune recognition
T2 - Proceedings of the National Academy of Sciences of the United States of America
UR - http://dx.doi.org/10.1073/pnas.2002759117
UR - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000530099500065&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR - https://www.pnas.org/content/117/17/9613
UR - http://hdl.handle.net/10044/1/87427
VL - 117
ER -