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The woody plant-degrading pathogen Lasiodiplodia theobromae effector LtCre1 targets the grapevine sugar-signaling protein VvRHIP1 to suppress host immunity

Lasiodiplodia theobromae is a causal agent of Botryosphaeria dieback, which seriously threatens grapevine production worldwide. Plant pathogens secrete diverse effectors to suppress host immune responses and promote the progression of infection, but the mechanisms underlying the manipulation of host...

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Autores principales: Xing, Qikai, Zhou, Xiangui, Cao, Yang, Peng, Junbo, Zhang, Wei, Wang, Xuncheng, Wu, Jiahong, Li, Xinghong, Yan, Jiye
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10112684/
https://www.ncbi.nlm.nih.gov/pubmed/36788641
http://dx.doi.org/10.1093/jxb/erad055
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author Xing, Qikai
Zhou, Xiangui
Cao, Yang
Peng, Junbo
Zhang, Wei
Wang, Xuncheng
Wu, Jiahong
Li, Xinghong
Yan, Jiye
author_facet Xing, Qikai
Zhou, Xiangui
Cao, Yang
Peng, Junbo
Zhang, Wei
Wang, Xuncheng
Wu, Jiahong
Li, Xinghong
Yan, Jiye
author_sort Xing, Qikai
collection PubMed
description Lasiodiplodia theobromae is a causal agent of Botryosphaeria dieback, which seriously threatens grapevine production worldwide. Plant pathogens secrete diverse effectors to suppress host immune responses and promote the progression of infection, but the mechanisms underlying the manipulation of host immunity by L. theobromae effectors are poorly understood. In this study, we characterized LtCre1, which encodes a L. theobromae effector that suppresses BAX-triggered cell death in Nicotiana benthamiana. RNAi-silencing and overexpression of LtCre1 in L. theobromae showed impaired and increased virulence, respectively, and ectopic expression in N. benthamiana increased susceptibility. These results suggest that LtCre1 is as an essential virulence factor for L. theobromae. Protein–protein interaction studies revealed that LtCre1 interacts with grapevine RGS1-HXK1-interacting protein 1 (VvRHIP1). Ectopic overexpression of VvRHIP1 in N. benthamiana reduced infection, suggesting that VvRHIP1 enhances plant immunity against L. theobromae. LtCre1 was found to disrupt the formation of the VvRHIP1–VvRGS1 complex and to participate in regulating the plant sugar-signaling pathway. Thus, our results suggest that L. theobromae LtCre1 targets the grapevine VvRHIP1 protein to manipulate the sugar-signaling pathway by disrupting the association of the VvRHIP1–VvRGS1 complex.
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spelling pubmed-101126842023-04-19 The woody plant-degrading pathogen Lasiodiplodia theobromae effector LtCre1 targets the grapevine sugar-signaling protein VvRHIP1 to suppress host immunity Xing, Qikai Zhou, Xiangui Cao, Yang Peng, Junbo Zhang, Wei Wang, Xuncheng Wu, Jiahong Li, Xinghong Yan, Jiye J Exp Bot Research Papers Lasiodiplodia theobromae is a causal agent of Botryosphaeria dieback, which seriously threatens grapevine production worldwide. Plant pathogens secrete diverse effectors to suppress host immune responses and promote the progression of infection, but the mechanisms underlying the manipulation of host immunity by L. theobromae effectors are poorly understood. In this study, we characterized LtCre1, which encodes a L. theobromae effector that suppresses BAX-triggered cell death in Nicotiana benthamiana. RNAi-silencing and overexpression of LtCre1 in L. theobromae showed impaired and increased virulence, respectively, and ectopic expression in N. benthamiana increased susceptibility. These results suggest that LtCre1 is as an essential virulence factor for L. theobromae. Protein–protein interaction studies revealed that LtCre1 interacts with grapevine RGS1-HXK1-interacting protein 1 (VvRHIP1). Ectopic overexpression of VvRHIP1 in N. benthamiana reduced infection, suggesting that VvRHIP1 enhances plant immunity against L. theobromae. LtCre1 was found to disrupt the formation of the VvRHIP1–VvRGS1 complex and to participate in regulating the plant sugar-signaling pathway. Thus, our results suggest that L. theobromae LtCre1 targets the grapevine VvRHIP1 protein to manipulate the sugar-signaling pathway by disrupting the association of the VvRHIP1–VvRGS1 complex. Oxford University Press 2023-02-15 /pmc/articles/PMC10112684/ /pubmed/36788641 http://dx.doi.org/10.1093/jxb/erad055 Text en © The Author(s) 2023. Published by Oxford University Press on behalf of the Society for Experimental Biology. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Papers
Xing, Qikai
Zhou, Xiangui
Cao, Yang
Peng, Junbo
Zhang, Wei
Wang, Xuncheng
Wu, Jiahong
Li, Xinghong
Yan, Jiye
The woody plant-degrading pathogen Lasiodiplodia theobromae effector LtCre1 targets the grapevine sugar-signaling protein VvRHIP1 to suppress host immunity
title The woody plant-degrading pathogen Lasiodiplodia theobromae effector LtCre1 targets the grapevine sugar-signaling protein VvRHIP1 to suppress host immunity
title_full The woody plant-degrading pathogen Lasiodiplodia theobromae effector LtCre1 targets the grapevine sugar-signaling protein VvRHIP1 to suppress host immunity
title_fullStr The woody plant-degrading pathogen Lasiodiplodia theobromae effector LtCre1 targets the grapevine sugar-signaling protein VvRHIP1 to suppress host immunity
title_full_unstemmed The woody plant-degrading pathogen Lasiodiplodia theobromae effector LtCre1 targets the grapevine sugar-signaling protein VvRHIP1 to suppress host immunity
title_short The woody plant-degrading pathogen Lasiodiplodia theobromae effector LtCre1 targets the grapevine sugar-signaling protein VvRHIP1 to suppress host immunity
title_sort woody plant-degrading pathogen lasiodiplodia theobromae effector ltcre1 targets the grapevine sugar-signaling protein vvrhip1 to suppress host immunity
topic Research Papers
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10112684/
https://www.ncbi.nlm.nih.gov/pubmed/36788641
http://dx.doi.org/10.1093/jxb/erad055
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