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Ac/Ds-Induced Receptor-like Kinase Genes Deletion Provides Broad-Spectrum Resistance to Bacterial Blight in Rice
Rice bacterial blight caused by Xanthomonas oryzae pv. oryzae (Xoo) seriously affects rice yield production. The discovery and application of broad-spectrum resistance genes are of great advance for disease resistance breeding. Previously, we identified that multiple receptor-like kinase (RLK) famil...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9103808/ https://www.ncbi.nlm.nih.gov/pubmed/35562952 http://dx.doi.org/10.3390/ijms23094561 |
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author | Mei, Qiong Fu, Yu Wen Li, Tian Miao Xuan, Yuan Hu |
author_facet | Mei, Qiong Fu, Yu Wen Li, Tian Miao Xuan, Yuan Hu |
author_sort | Mei, Qiong |
collection | PubMed |
description | Rice bacterial blight caused by Xanthomonas oryzae pv. oryzae (Xoo) seriously affects rice yield production. The discovery and application of broad-spectrum resistance genes are of great advance for disease resistance breeding. Previously, we identified that multiple receptor-like kinase (RLK) family gene deletions induced by the Ac/Ds system resulted in a lesion mimic symptom. In this study, the mutant #29 showed that this lesion mimic symptom was isolated. Further analysis identified that four RLK genes (RLK19-22) were deleted in the #29 mutant. The #29 mutant exhibited broad-spectrum resistance to Xoo and subsequent analyses identified that pathogenesis-related genes PR1a, PBZ1, and cellular H(2)O(2) levels were significantly induced in the mutant compared to wild-type plants. A genetic analysis revealed that reconstruction of RLK20, RLK21, or RLK22 rescued the lesion mimic symptom of the #29 mutant, indicating that these three RLKs are responsible for broad-spectrum resistance in rice. Further yeast two hybrid and bimolecular fluorescence complementation assays demonstrated that RLK20 interacts with RBOHB, which is a ROS producer in plants. Compared to wild-type plants, the #29 mutant was more, while #29/RLK20 ox was less, susceptible to MV (methyl-viologen), an ROS inducer. Co-expression of RLK20 and RBOHB reduced RBOHB-promoted H(2)O(2) accumulation in the cells. Taken together, our research indicated that the RLKs may inhibit RBOHB activity to negatively regulate rice resistance to Xoo. These results provide the theoretical basis and valuable information about the target genes necessary for the successful breeding of rice cultivars resistant to bacterial blight. |
format | Online Article Text |
id | pubmed-9103808 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-91038082022-05-14 Ac/Ds-Induced Receptor-like Kinase Genes Deletion Provides Broad-Spectrum Resistance to Bacterial Blight in Rice Mei, Qiong Fu, Yu Wen Li, Tian Miao Xuan, Yuan Hu Int J Mol Sci Article Rice bacterial blight caused by Xanthomonas oryzae pv. oryzae (Xoo) seriously affects rice yield production. The discovery and application of broad-spectrum resistance genes are of great advance for disease resistance breeding. Previously, we identified that multiple receptor-like kinase (RLK) family gene deletions induced by the Ac/Ds system resulted in a lesion mimic symptom. In this study, the mutant #29 showed that this lesion mimic symptom was isolated. Further analysis identified that four RLK genes (RLK19-22) were deleted in the #29 mutant. The #29 mutant exhibited broad-spectrum resistance to Xoo and subsequent analyses identified that pathogenesis-related genes PR1a, PBZ1, and cellular H(2)O(2) levels were significantly induced in the mutant compared to wild-type plants. A genetic analysis revealed that reconstruction of RLK20, RLK21, or RLK22 rescued the lesion mimic symptom of the #29 mutant, indicating that these three RLKs are responsible for broad-spectrum resistance in rice. Further yeast two hybrid and bimolecular fluorescence complementation assays demonstrated that RLK20 interacts with RBOHB, which is a ROS producer in plants. Compared to wild-type plants, the #29 mutant was more, while #29/RLK20 ox was less, susceptible to MV (methyl-viologen), an ROS inducer. Co-expression of RLK20 and RBOHB reduced RBOHB-promoted H(2)O(2) accumulation in the cells. Taken together, our research indicated that the RLKs may inhibit RBOHB activity to negatively regulate rice resistance to Xoo. These results provide the theoretical basis and valuable information about the target genes necessary for the successful breeding of rice cultivars resistant to bacterial blight. MDPI 2022-04-20 /pmc/articles/PMC9103808/ /pubmed/35562952 http://dx.doi.org/10.3390/ijms23094561 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Mei, Qiong Fu, Yu Wen Li, Tian Miao Xuan, Yuan Hu Ac/Ds-Induced Receptor-like Kinase Genes Deletion Provides Broad-Spectrum Resistance to Bacterial Blight in Rice |
title | Ac/Ds-Induced Receptor-like Kinase Genes Deletion Provides Broad-Spectrum Resistance to Bacterial Blight in Rice |
title_full | Ac/Ds-Induced Receptor-like Kinase Genes Deletion Provides Broad-Spectrum Resistance to Bacterial Blight in Rice |
title_fullStr | Ac/Ds-Induced Receptor-like Kinase Genes Deletion Provides Broad-Spectrum Resistance to Bacterial Blight in Rice |
title_full_unstemmed | Ac/Ds-Induced Receptor-like Kinase Genes Deletion Provides Broad-Spectrum Resistance to Bacterial Blight in Rice |
title_short | Ac/Ds-Induced Receptor-like Kinase Genes Deletion Provides Broad-Spectrum Resistance to Bacterial Blight in Rice |
title_sort | ac/ds-induced receptor-like kinase genes deletion provides broad-spectrum resistance to bacterial blight in rice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9103808/ https://www.ncbi.nlm.nih.gov/pubmed/35562952 http://dx.doi.org/10.3390/ijms23094561 |
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