CHIMERIC FLORAL ORGANS1, Encoding a Monocot-Specific MADS Box Protein, Regulates Floral Organ Identity in Rice

CHIMERIC FLORAL ORGANS1, Encoding a Monocot-Specific MADS Box Protein, Regulates Floral Organ Identity in Rice
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嵌合花器官1,编码单子叶植物特异性MADS盒蛋白,调节水稻花器官的特性

DOI:
10.1104/pp.112.200980
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发表时间:
2012-10-01
期刊:
影响因子:
7.4
通讯作者:
He, Guanghua
He, Guanghua
中科院分区:
生物学1区
文献类型:
--
作者:
Sang, Xianchun;Li, Yunfeng;He, Guanghua

文献摘要

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同源异型MADS盒基因控制真双子叶植物花器官的同一性。然而,禾本科植物具有高度特化的外部花器官,并且调节禾本科植物高度特化的外部花器官的基因的身份仍然不清楚。在这项研究中,我们的特点是MIKC型MADS盒基因,嵌合花器官(CFO 1),它在调控花器官的身份在水稻(Oryza sativa)的关键作用。cfo 1突变体显示有缺陷的边缘区域的内稃,嵌合花器官,和异位花器官。图位克隆结果表明,CFO 1编码OsMADS 32蛋白。系统进化分析表明,CFO 1/OsMADS 32属于MIKC型MADS盒基因家族中的一个单子叶植物特异分支。CFO 1的表达区域主要局限于内稃边缘和花内器官。花器官特性基因DROOPING LEAF(DL)在cfo 1花的所有缺陷器官中异位表达。双突变体分析表明,DL功能的丧失减轻了cfo 1花器官的一些缺陷。我们认为CFO 1基因通过负调控DL表达在维持花器官同一性中起着关键作用。
The control of floral organ identity by homeotic MADS box genes is well established in eudicots. However, grasses have highly specialized outer floral organs, and the identities of the genes that regulate the highly specialized outer floral organs of grasses remain unclear. In this study, we characterized a MIKC-type MADS box gene, CHIMERIC FLORAL ORGANS (CFO1), which plays a key role in the regulation of floral organ identity in rice (Oryza sativa). The cfo1 mutant displayed defective marginal regions of the palea, chimeric floral organs, and ectopic floral organs. Map-based cloning demonstrated that CFO1 encoded the OsMADS32 protein. Phylogenetic analysis revealed that CFO1/OsMADS32 belonged to a monocot-specific clade in the MIKC-type MADS box gene family. The expression domains of CFO1 were mainly restricted to the marginal region of the palea and inner floral organs. The floral organ identity gene DROOPING LEAF (DL) was expressed ectopically in all defective organs of cfo1 flowers. Double mutant analysis revealed that loss of DL function mitigated some of the defects of floral organs in cfo1 flowers. We propose that the CFO1 gene plays a pivotal role in maintaining floral organ identity through negative regulation of DL expression.