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Disruption of OsPHD1, Encoding a UDP-Glucose Epimerase, Causes JA Accumulation and Enhanced Bacterial Blight Resistance in Rice

Lesion mimic mutants (LMMs) have been widely used in experiments in recent years for studying plant physiological mechanisms underlying programmed cell death (PCD) and defense responses. Here, we identified a lesion mimic mutant, lm212-1, which cloned the causal gene by a map-based cloning strategy,...

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Autores principales: Gao, Yu, Xiang, Xiaojiao, Zhang, Yingxin, Cao, Yongrun, Wang, Beifang, Zhang, Yue, Wang, Chen, Jiang, Min, Duan, Wenjing, Chen, Daibo, Zhan, Xiaodeng, Cheng, Shihua, Liu, Qunen, Cao, Liyong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8775874/
https://www.ncbi.nlm.nih.gov/pubmed/35054937
http://dx.doi.org/10.3390/ijms23020751
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author Gao, Yu
Xiang, Xiaojiao
Zhang, Yingxin
Cao, Yongrun
Wang, Beifang
Zhang, Yue
Wang, Chen
Jiang, Min
Duan, Wenjing
Chen, Daibo
Zhan, Xiaodeng
Cheng, Shihua
Liu, Qunen
Cao, Liyong
author_facet Gao, Yu
Xiang, Xiaojiao
Zhang, Yingxin
Cao, Yongrun
Wang, Beifang
Zhang, Yue
Wang, Chen
Jiang, Min
Duan, Wenjing
Chen, Daibo
Zhan, Xiaodeng
Cheng, Shihua
Liu, Qunen
Cao, Liyong
author_sort Gao, Yu
collection PubMed
description Lesion mimic mutants (LMMs) have been widely used in experiments in recent years for studying plant physiological mechanisms underlying programmed cell death (PCD) and defense responses. Here, we identified a lesion mimic mutant, lm212-1, which cloned the causal gene by a map-based cloning strategy, and verified this by complementation. The causal gene, OsPHD1, encodes a UDP-glucose epimerase (UGE), and the OsPHD1 was located in the chloroplast. OsPHD1 was constitutively expressed in all organs, with higher expression in leaves and other green tissues. lm212-1 exhibited decreased chlorophyll content, and the chloroplast structure was destroyed. Histochemistry results indicated that H(2)O(2) is highly accumulated and cell death is occurred around the lesions in lm212-1. Compared to the wild type, expression levels of defense-related genes were up-regulated, and resistance to bacterial pathogens Xanthomonas oryzae pv. oryzae (Xoo) was enhanced, indicating that the defense response was activated in lm212-1, ROS production was induced by flg22, and chitin treatment also showed the same result. Jasmonic acid (JA) and methyl jasmonate (MeJA) increased, and the JA signaling pathways appeared to be disordered in lm212-1. Additionally, the overexpression lines showed the same phenotype as the wild type. Overall, our findings demonstrate that OsPHD1 is involved in the regulation of PCD and defense response in rice.
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spelling pubmed-87758742022-01-21 Disruption of OsPHD1, Encoding a UDP-Glucose Epimerase, Causes JA Accumulation and Enhanced Bacterial Blight Resistance in Rice Gao, Yu Xiang, Xiaojiao Zhang, Yingxin Cao, Yongrun Wang, Beifang Zhang, Yue Wang, Chen Jiang, Min Duan, Wenjing Chen, Daibo Zhan, Xiaodeng Cheng, Shihua Liu, Qunen Cao, Liyong Int J Mol Sci Article Lesion mimic mutants (LMMs) have been widely used in experiments in recent years for studying plant physiological mechanisms underlying programmed cell death (PCD) and defense responses. Here, we identified a lesion mimic mutant, lm212-1, which cloned the causal gene by a map-based cloning strategy, and verified this by complementation. The causal gene, OsPHD1, encodes a UDP-glucose epimerase (UGE), and the OsPHD1 was located in the chloroplast. OsPHD1 was constitutively expressed in all organs, with higher expression in leaves and other green tissues. lm212-1 exhibited decreased chlorophyll content, and the chloroplast structure was destroyed. Histochemistry results indicated that H(2)O(2) is highly accumulated and cell death is occurred around the lesions in lm212-1. Compared to the wild type, expression levels of defense-related genes were up-regulated, and resistance to bacterial pathogens Xanthomonas oryzae pv. oryzae (Xoo) was enhanced, indicating that the defense response was activated in lm212-1, ROS production was induced by flg22, and chitin treatment also showed the same result. Jasmonic acid (JA) and methyl jasmonate (MeJA) increased, and the JA signaling pathways appeared to be disordered in lm212-1. Additionally, the overexpression lines showed the same phenotype as the wild type. Overall, our findings demonstrate that OsPHD1 is involved in the regulation of PCD and defense response in rice. MDPI 2022-01-11 /pmc/articles/PMC8775874/ /pubmed/35054937 http://dx.doi.org/10.3390/ijms23020751 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
Gao, Yu
Xiang, Xiaojiao
Zhang, Yingxin
Cao, Yongrun
Wang, Beifang
Zhang, Yue
Wang, Chen
Jiang, Min
Duan, Wenjing
Chen, Daibo
Zhan, Xiaodeng
Cheng, Shihua
Liu, Qunen
Cao, Liyong
Disruption of OsPHD1, Encoding a UDP-Glucose Epimerase, Causes JA Accumulation and Enhanced Bacterial Blight Resistance in Rice
title Disruption of OsPHD1, Encoding a UDP-Glucose Epimerase, Causes JA Accumulation and Enhanced Bacterial Blight Resistance in Rice
title_full Disruption of OsPHD1, Encoding a UDP-Glucose Epimerase, Causes JA Accumulation and Enhanced Bacterial Blight Resistance in Rice
title_fullStr Disruption of OsPHD1, Encoding a UDP-Glucose Epimerase, Causes JA Accumulation and Enhanced Bacterial Blight Resistance in Rice
title_full_unstemmed Disruption of OsPHD1, Encoding a UDP-Glucose Epimerase, Causes JA Accumulation and Enhanced Bacterial Blight Resistance in Rice
title_short Disruption of OsPHD1, Encoding a UDP-Glucose Epimerase, Causes JA Accumulation and Enhanced Bacterial Blight Resistance in Rice
title_sort disruption of osphd1, encoding a udp-glucose epimerase, causes ja accumulation and enhanced bacterial blight resistance in rice
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8775874/
https://www.ncbi.nlm.nih.gov/pubmed/35054937
http://dx.doi.org/10.3390/ijms23020751
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