A SNP in OsMCA1 responding for a plant architecture defect by deactivation of bioactive GA in rice
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- 作者：Zhenwei Liu (1)
Qin Cheng (1)
Yunfang Sun (1)
Huixia Dai (1)
Gaoyuan Song (1)
Zhibin Guo (1)
Xuefeng Qu (1)
Daiming Jiang (1)
Chuan Liu (1)
Wei Wang (1)
Daichang Yang (1) - 关键词：Internode elongation ; GA biosynthesis ; GA deactivation ; Map ; based cloning ; Plant architecture ; Plant height ; Rice pad mutant
- 刊名：Plant Molecular Biology
- 出版年：2015
- 出版时间：January 2015
- 年：2015
- 卷：87
- 期：1-2
- 页码：17-30
- 全文大小：5,665 KB
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Qin Cheng (1)
Yunfang Sun (1)
Huixia Dai (1)
Gaoyuan Song (1)
Zhibin Guo (1)
Xuefeng Qu (1)
Daiming Jiang (1)
Chuan Liu (1)
Wei Wang (1)
Daichang Yang (1)
1. State Key Laboratory of Hybrid Rice, College of Life Sciences, Wuhan University, Luojia Hill, Wuhan, 430072, Hubei Province, China - ISSN：1573-5028
文摘
Plant architecture directly affects biomass in higher plants, especially grain yields in agricultural crops. In this study, we characterized a recessive mutant, plant architecture determinant (pad), derived from the Oryza sativa ssp. indica cultivar MH86. The mutant exhibited severe dwarf phenotypes, including shorter and stunted leaves, fewer secondary branches during both the vegetative and reproductive growth stages. Cytological studies revealed that pad mutant growth defects are primarily due to the inhibition of cell expansion. The PAD gene was isolated using a map-based cloning strategy. It encodes a plasma membrane protein OsMCA1 and a SNP responsible for a single amino acid change was found in the mutant. PAD was universally expressed in rice tissues from the vegetative to reproductive growth stages, especially in seedlings, nodes and rachillae. Quantitative real-time PCR analysis revealed that the most of the genes responding to gibberellin (GA) metabolism were up-regulated in pad mutant internodes. The endogenous GA content measurement revealed that the levels of GA1 were significantly decreased in the third internode of pad mutants. Moreover, a GA response assay suggested that OsMCA1/PAD might be involved in the regulation of GA metabolism and signal transduction. Our results revealed the pad is a loss-of-function mutant of the OsMCA1/PAD, leading to upregulation of genes related to GA deactivation, which decreased bioactive GA levels.