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Genome-wide association studies identify OsWRKY53 as a key regulator of salt tolerance in rice
Salinity stress progressively reduces plant growth and productivity, while plant has developed complex signaling pathways to confront salt stress. However, only a few genetic variants have been identified to mediate salt tolerance in the major crop rice, and the molecular mechanism remains poorly un...
Autores principales: | , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10272163/ https://www.ncbi.nlm.nih.gov/pubmed/37321989 http://dx.doi.org/10.1038/s41467-023-39167-0 |
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author | Yu, Jun Zhu, Chengsong Xuan, Wei An, Hongzhou Tian, Yunlu Wang, Baoxiang Chi, Wenchao Chen, Gaoming Ge, Yuwei Li, Jin Dai, Zhaoyang Liu, Yan Sun, Zhiguang Xu, Dayong Wang, Chunming Wan, Jianmin |
author_facet | Yu, Jun Zhu, Chengsong Xuan, Wei An, Hongzhou Tian, Yunlu Wang, Baoxiang Chi, Wenchao Chen, Gaoming Ge, Yuwei Li, Jin Dai, Zhaoyang Liu, Yan Sun, Zhiguang Xu, Dayong Wang, Chunming Wan, Jianmin |
author_sort | Yu, Jun |
collection | PubMed |
description | Salinity stress progressively reduces plant growth and productivity, while plant has developed complex signaling pathways to confront salt stress. However, only a few genetic variants have been identified to mediate salt tolerance in the major crop rice, and the molecular mechanism remains poorly understood. Here, we identify ten candidate genes associated with salt-tolerance (ST) traits by performing a genome-wide association analysis in rice landraces. We characterize two ST-related genes, encoding transcriptional factor OsWRKY53 and Mitogen-activated protein Kinase Kinase OsMKK10.2, that mediate root Na(+) flux and Na(+) homeostasis. We further find that OsWRKY53 acts as a negative modulator regulating expression of OsMKK10.2 in promoting ion homeostasis. Furthermore, OsWRKY53 trans-represses OsHKT1;5 (high-affinity K(+) transporter 1;5), encoding a sodium transport protein in roots. We show that the OsWRKY53-OsMKK10.2 and OsWRKY53-OsHKT1;5 module coordinate defenses against ionic stress. The results shed light on the regulatory mechanisms underlying plant salt tolerance. |
format | Online Article Text |
id | pubmed-10272163 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-102721632023-06-17 Genome-wide association studies identify OsWRKY53 as a key regulator of salt tolerance in rice Yu, Jun Zhu, Chengsong Xuan, Wei An, Hongzhou Tian, Yunlu Wang, Baoxiang Chi, Wenchao Chen, Gaoming Ge, Yuwei Li, Jin Dai, Zhaoyang Liu, Yan Sun, Zhiguang Xu, Dayong Wang, Chunming Wan, Jianmin Nat Commun Article Salinity stress progressively reduces plant growth and productivity, while plant has developed complex signaling pathways to confront salt stress. However, only a few genetic variants have been identified to mediate salt tolerance in the major crop rice, and the molecular mechanism remains poorly understood. Here, we identify ten candidate genes associated with salt-tolerance (ST) traits by performing a genome-wide association analysis in rice landraces. We characterize two ST-related genes, encoding transcriptional factor OsWRKY53 and Mitogen-activated protein Kinase Kinase OsMKK10.2, that mediate root Na(+) flux and Na(+) homeostasis. We further find that OsWRKY53 acts as a negative modulator regulating expression of OsMKK10.2 in promoting ion homeostasis. Furthermore, OsWRKY53 trans-represses OsHKT1;5 (high-affinity K(+) transporter 1;5), encoding a sodium transport protein in roots. We show that the OsWRKY53-OsMKK10.2 and OsWRKY53-OsHKT1;5 module coordinate defenses against ionic stress. The results shed light on the regulatory mechanisms underlying plant salt tolerance. Nature Publishing Group UK 2023-06-15 /pmc/articles/PMC10272163/ /pubmed/37321989 http://dx.doi.org/10.1038/s41467-023-39167-0 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Yu, Jun Zhu, Chengsong Xuan, Wei An, Hongzhou Tian, Yunlu Wang, Baoxiang Chi, Wenchao Chen, Gaoming Ge, Yuwei Li, Jin Dai, Zhaoyang Liu, Yan Sun, Zhiguang Xu, Dayong Wang, Chunming Wan, Jianmin Genome-wide association studies identify OsWRKY53 as a key regulator of salt tolerance in rice |
title | Genome-wide association studies identify OsWRKY53 as a key regulator of salt tolerance in rice |
title_full | Genome-wide association studies identify OsWRKY53 as a key regulator of salt tolerance in rice |
title_fullStr | Genome-wide association studies identify OsWRKY53 as a key regulator of salt tolerance in rice |
title_full_unstemmed | Genome-wide association studies identify OsWRKY53 as a key regulator of salt tolerance in rice |
title_short | Genome-wide association studies identify OsWRKY53 as a key regulator of salt tolerance in rice |
title_sort | genome-wide association studies identify oswrky53 as a key regulator of salt tolerance in rice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10272163/ https://www.ncbi.nlm.nih.gov/pubmed/37321989 http://dx.doi.org/10.1038/s41467-023-39167-0 |
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