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Gibberellin Biosynthetic Deficiency Is Responsible for Maize Dominant Dwarf11 (D11) Mutant Phenotype: Physiological and Transcriptomic Evidence
Dwarf stature is introduced to improve lodging resistance and harvest index in crop production. In many crops including maize, mining and application of novel dwarf genes are urgent to overcome genetic bottleneck and vulnerability during breeding improvement. Here we report the characterization and...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3680376/ https://www.ncbi.nlm.nih.gov/pubmed/23776674 http://dx.doi.org/10.1371/journal.pone.0066466 |
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author | Wang, Yijun Deng, Dexiang Ding, Haidong Xu, Xiangming Zhang, Rong Wang, Suxin Bian, Yunlong Yin, Zhitong Chen, Yao |
author_facet | Wang, Yijun Deng, Dexiang Ding, Haidong Xu, Xiangming Zhang, Rong Wang, Suxin Bian, Yunlong Yin, Zhitong Chen, Yao |
author_sort | Wang, Yijun |
collection | PubMed |
description | Dwarf stature is introduced to improve lodging resistance and harvest index in crop production. In many crops including maize, mining and application of novel dwarf genes are urgent to overcome genetic bottleneck and vulnerability during breeding improvement. Here we report the characterization and expression profiling analysis of a newly identified maize dwarf mutant Dwarf11 (D11). The D11 displays severely developmental abnormalities and is controlled by a dominant Mendelian factor. The D11 seedlings responds to both GA(3) and paclobutrazol (PAC) application, suggesting that dwarf phenotype of D11 is caused by GA biosynthesis instead of GA signaling deficiency. In contrast, two well-characterized maize dominant dwarf plants D8 and D9 are all insensitive to exogenous GA(3) stimulation. Additionally, sequence variation of D8 and D9 genes was not identified in the D11 mutant. Microarray and qRT-PCR analysis results demonstrated that transcripts encoding GA biosynthetic and catabolic enzymes ent-kaurenoic acid oxidase (KAO), GA 20-oxidase (GA20ox), and GA 2-oxidase (GA2ox) are up-regulated in D11. Our results lay a foundation for the following D11 gene cloning and functional characterization. Moreover, results presented here may aid in crops molecular improvement and breeding, especially breeding of crops with plant height ideotypes. |
format | Online Article Text |
id | pubmed-3680376 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-36803762013-06-17 Gibberellin Biosynthetic Deficiency Is Responsible for Maize Dominant Dwarf11 (D11) Mutant Phenotype: Physiological and Transcriptomic Evidence Wang, Yijun Deng, Dexiang Ding, Haidong Xu, Xiangming Zhang, Rong Wang, Suxin Bian, Yunlong Yin, Zhitong Chen, Yao PLoS One Research Article Dwarf stature is introduced to improve lodging resistance and harvest index in crop production. In many crops including maize, mining and application of novel dwarf genes are urgent to overcome genetic bottleneck and vulnerability during breeding improvement. Here we report the characterization and expression profiling analysis of a newly identified maize dwarf mutant Dwarf11 (D11). The D11 displays severely developmental abnormalities and is controlled by a dominant Mendelian factor. The D11 seedlings responds to both GA(3) and paclobutrazol (PAC) application, suggesting that dwarf phenotype of D11 is caused by GA biosynthesis instead of GA signaling deficiency. In contrast, two well-characterized maize dominant dwarf plants D8 and D9 are all insensitive to exogenous GA(3) stimulation. Additionally, sequence variation of D8 and D9 genes was not identified in the D11 mutant. Microarray and qRT-PCR analysis results demonstrated that transcripts encoding GA biosynthetic and catabolic enzymes ent-kaurenoic acid oxidase (KAO), GA 20-oxidase (GA20ox), and GA 2-oxidase (GA2ox) are up-regulated in D11. Our results lay a foundation for the following D11 gene cloning and functional characterization. Moreover, results presented here may aid in crops molecular improvement and breeding, especially breeding of crops with plant height ideotypes. Public Library of Science 2013-06-12 /pmc/articles/PMC3680376/ /pubmed/23776674 http://dx.doi.org/10.1371/journal.pone.0066466 Text en © 2013 Wang et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Wang, Yijun Deng, Dexiang Ding, Haidong Xu, Xiangming Zhang, Rong Wang, Suxin Bian, Yunlong Yin, Zhitong Chen, Yao Gibberellin Biosynthetic Deficiency Is Responsible for Maize Dominant Dwarf11 (D11) Mutant Phenotype: Physiological and Transcriptomic Evidence |
title | Gibberellin Biosynthetic Deficiency Is Responsible for Maize Dominant Dwarf11 (D11) Mutant Phenotype: Physiological and Transcriptomic Evidence |
title_full | Gibberellin Biosynthetic Deficiency Is Responsible for Maize Dominant Dwarf11 (D11) Mutant Phenotype: Physiological and Transcriptomic Evidence |
title_fullStr | Gibberellin Biosynthetic Deficiency Is Responsible for Maize Dominant Dwarf11 (D11) Mutant Phenotype: Physiological and Transcriptomic Evidence |
title_full_unstemmed | Gibberellin Biosynthetic Deficiency Is Responsible for Maize Dominant Dwarf11 (D11) Mutant Phenotype: Physiological and Transcriptomic Evidence |
title_short | Gibberellin Biosynthetic Deficiency Is Responsible for Maize Dominant Dwarf11 (D11) Mutant Phenotype: Physiological and Transcriptomic Evidence |
title_sort | gibberellin biosynthetic deficiency is responsible for maize dominant dwarf11 (d11) mutant phenotype: physiological and transcriptomic evidence |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3680376/ https://www.ncbi.nlm.nih.gov/pubmed/23776674 http://dx.doi.org/10.1371/journal.pone.0066466 |
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