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SHALLOT-LIKE1 Is a KANADI Transcription Factor That Modulates Rice Leaf Rolling by Regulating Leaf Abaxial Cell Development

机译:香葱样1是一种通过调节叶片释放细胞开发来调节稻壳轧制的Kanadi转录因子

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As an important agronomic trait, rice (Oryza sativa L.) leaf rolling has attracted much attention from plant biologists and breeders. Moderate leaf rolling increases the photosynthesis of cultivars and hence raises grain yield. However, the relevant molecular mechanism remains unclear. Here, we show the isolation and functional characterization of SHALLOT-LIKE1 (SLL1), a key gene controlling rice leaf rolling. sll1 mutant plants have extremely incurved leaves due to the defective development of sclerenchymatous cells on the abaxial side. Defective development can be functionally rescued by expression of SLL1. SLL1 is transcribed in various tissues and accumulates in the abaxial epidermis throughout leaf development. SLL1 encodes a SHAQKYF class MYB family transcription factor belonging to the KANADI family. SLL1 deficiency leads to defective programmed cell death of abaxial mesophyll cells and suppresses the development of abaxial features. By contrast, enhanced SLL1 expression stimulates phloem development on the abaxial side and suppresses bulliform cell and sclerenchyma development on the adaxial side. Additionally, SLL1 deficiency results in increased chlorophyll and photosynthesis. Our findings identify the role of SLL1 in the modulation of leaf abaxial cell development and in sustaining abaxial characteristics during leaf development. These results should facilitate attempts to use molecular breeding to increase the photosynthetic capacity of rice, as well as other crops, by modulating leaf development and rolling.
机译:作为一个重要的农艺性状,稻米(Oryza Sativa L.)叶滚动引起了植物生物学家和饲养员的许多关注。中等叶片轧制增加了品种的光合作用,因此提高了籽粒产量。但是,相关的分子机制仍然不清楚。在这里,我们展示了浅鳞状物(SLL1)的隔离和功能表征,是控制米叶轧制的关键基因。由于在亚轴侧的硬化细胞缺陷的发育,SLL1突变植物具有极大的叶片。通过表达SLL1可以在功能救出有缺陷的发展。 SLL1在各种组织中转录,并在整个叶片发育中累积在叶形表皮中。 SLL1编码属于Kanadi家族的Shaqkyf类MyB系列转录因子。 SLL1缺乏导致有缺陷的缺陷叶片细胞的细胞死亡,并抑制了缺点特征的发展。相比之下,增强型SLL1表达刺激了在轴向侧的韧皮肌发育,抑制了对侧侧的牛状细胞和硬化血液发育。此外,SLL1缺乏导致叶绿素和光合作用增加。我们的研究结果识别SLL1在叶子释录细胞开发调节中的作用及叶片发育过程中的遗传特征。这些结果应通过调节叶片发育和轧制来促进使用分子育种来增加水稻和其他作物的光合容量。

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