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XopZ and ORP1C cooperate to regulate the virulence of Xanthomonas oryzae pv. oryzae on Nipponbare
Bacterial leaf blight caused by Xanthomonas oryzae pv. oryzae (Xoo) has always been considered to be one of the most severe worldwide diseases in rice. Xoo strains usually use the highly conserved type III secretion system (T3SS) to deliver virulence effectors into rice cells and further suppress th...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8959505/ https://www.ncbi.nlm.nih.gov/pubmed/35184695 http://dx.doi.org/10.1080/15592324.2022.2035126 |
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author | Ji, Hongtao Li, Taoran Li, Xiaochen Li, Jiangyu Yu, Jiayi Zhang, Xin Liu, Delong |
author_facet | Ji, Hongtao Li, Taoran Li, Xiaochen Li, Jiangyu Yu, Jiayi Zhang, Xin Liu, Delong |
author_sort | Ji, Hongtao |
collection | PubMed |
description | Bacterial leaf blight caused by Xanthomonas oryzae pv. oryzae (Xoo) has always been considered to be one of the most severe worldwide diseases in rice. Xoo strains usually use the highly conserved type III secretion system (T3SS) to deliver virulence effectors into rice cells and further suppress the host’s immunity. Previous studies reported that different Xanthomonas outer protein (Xop) effectors include XopZ from one strain appear to share functional redundancies on suppressing rice PAMP-triggered immunity (PTI). But only xopZ, except other xop genes, could significantly impaire Xoo virulence when individually deleting in PXO99 strains. Thus, the XopZ effector should not only suppress rice PTI pathway, but also has other unknown indispensable pathological functions in PXO99–rice interactions. Here, we also found that ∆xopZ mutant strains displayed lower virulence on Nipponbare leaves compared with PXO99 strains. We identified an oxysterol-binding related protein, ORP1C, as a XopZ-interacting protein in rice. Further studies found that rice ORP1C preliminarily played a positive role in regulating the resistance to PXO99 strains, and XopZ–ORP1C interactions cooperated to regulate the compatible interactions of PXO99-Nipponbare rice. The reactive oxygen species (ROS) burst and PTI marker gene expression data indicated that ORP1C were not directly relevant to the PTI pathway in rice. The deeper mechanisms underlying XopZ–ORP1C interaction and how XopZ and ORP1C cooperate for regulating the PXO99–rice interactions require further exploration. |
format | Online Article Text |
id | pubmed-8959505 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-89595052022-03-29 XopZ and ORP1C cooperate to regulate the virulence of Xanthomonas oryzae pv. oryzae on Nipponbare Ji, Hongtao Li, Taoran Li, Xiaochen Li, Jiangyu Yu, Jiayi Zhang, Xin Liu, Delong Plant Signal Behav Short Communication Bacterial leaf blight caused by Xanthomonas oryzae pv. oryzae (Xoo) has always been considered to be one of the most severe worldwide diseases in rice. Xoo strains usually use the highly conserved type III secretion system (T3SS) to deliver virulence effectors into rice cells and further suppress the host’s immunity. Previous studies reported that different Xanthomonas outer protein (Xop) effectors include XopZ from one strain appear to share functional redundancies on suppressing rice PAMP-triggered immunity (PTI). But only xopZ, except other xop genes, could significantly impaire Xoo virulence when individually deleting in PXO99 strains. Thus, the XopZ effector should not only suppress rice PTI pathway, but also has other unknown indispensable pathological functions in PXO99–rice interactions. Here, we also found that ∆xopZ mutant strains displayed lower virulence on Nipponbare leaves compared with PXO99 strains. We identified an oxysterol-binding related protein, ORP1C, as a XopZ-interacting protein in rice. Further studies found that rice ORP1C preliminarily played a positive role in regulating the resistance to PXO99 strains, and XopZ–ORP1C interactions cooperated to regulate the compatible interactions of PXO99-Nipponbare rice. The reactive oxygen species (ROS) burst and PTI marker gene expression data indicated that ORP1C were not directly relevant to the PTI pathway in rice. The deeper mechanisms underlying XopZ–ORP1C interaction and how XopZ and ORP1C cooperate for regulating the PXO99–rice interactions require further exploration. Taylor & Francis 2022-02-19 /pmc/articles/PMC8959505/ /pubmed/35184695 http://dx.doi.org/10.1080/15592324.2022.2035126 Text en © 2022 The Author(s). Published with license by Taylor & Francis Group, LLC. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Short Communication Ji, Hongtao Li, Taoran Li, Xiaochen Li, Jiangyu Yu, Jiayi Zhang, Xin Liu, Delong XopZ and ORP1C cooperate to regulate the virulence of Xanthomonas oryzae pv. oryzae on Nipponbare |
title | XopZ and ORP1C cooperate to regulate the virulence of Xanthomonas oryzae pv. oryzae on Nipponbare |
title_full | XopZ and ORP1C cooperate to regulate the virulence of Xanthomonas oryzae pv. oryzae on Nipponbare |
title_fullStr | XopZ and ORP1C cooperate to regulate the virulence of Xanthomonas oryzae pv. oryzae on Nipponbare |
title_full_unstemmed | XopZ and ORP1C cooperate to regulate the virulence of Xanthomonas oryzae pv. oryzae on Nipponbare |
title_short | XopZ and ORP1C cooperate to regulate the virulence of Xanthomonas oryzae pv. oryzae on Nipponbare |
title_sort | xopz and orp1c cooperate to regulate the virulence of xanthomonas oryzae pv. oryzae on nipponbare |
topic | Short Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8959505/ https://www.ncbi.nlm.nih.gov/pubmed/35184695 http://dx.doi.org/10.1080/15592324.2022.2035126 |
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