Mutations in the MIT3 gene encoding a caroteniod isomerase lead to increased tiller number in rice.
Mutations in the MIT3 gene encoding a caroteniod isomerase lead to increased tiller number in rice.
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DOI：
10.1016/j.plantsci.2017.11.001
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发表时间：
2018-02
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通讯作者：
Lihua Liu;Tingting Xie;Peng Peng-Peng;Haiyang Qiu;Jinfeng Zhao;Jingjing Fang;S. Patil;Yiqin Wang;Shuang Fang;Jinfang Chu;Shoujiang Yuan;Wenhui Zhang;Xueyong Li
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文献类型：
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作者：
Lihua Liu;Tingting Xie;Peng Peng-Peng;Haiyang Qiu;Jinfeng Zhao;Jingjing Fang;S. Patil;Yiqin Wang;Shuang Fang;Jinfang Chu;Shoujiang Yuan;Wenhui Zhang;Xueyong Li
类胡萝卜素不仅在光收集和光保护中发挥重要作用，防止过量光照，而且还可以作为脱落酸 (ABA) 和独脚金内酯 (SL) 等阿朴胡萝卜素激素的前体。尽管类胡萝卜素生物合成突变体（如白化、叶片杂色和收获前发芽）的光和 ABA 相关表型已被广泛研究，但 SLs 相关的分枝表型却很少被探索。在这里，我们鉴定了四种名为mit3的等位基因水稻突变体，其表现出分蘖数适度增加、半矮化和叶片杂色。基于图谱的克隆表明，MIT3编码类胡萝卜素异构酶（CRTISO），这是类胡萝卜素生物合成中催化从前番茄红素到全反式番茄红素转化的关键酶。在黑暗生长的 mit3 幼苗中积累了前番茄红素，而几乎检测不到全反式番茄红素。因此，两种最丰富的类胡萝卜素——叶黄素和β-胡萝卜素的含量显着降低。此外，mit3中天然SL的epi-5DS含量显着降低。外源施用合成SL的GR24可以挽救mit3的分蘖表型。对mit3与SLs生物合成突变体d17的双突变分析表明，MIT3控制SLs生物合成途径上游的分蘖发育。我们的结果表明，mit3 的分蘖表型是由于 SL 缺乏造成的，并且类胡萝卜素缺乏与 SL 调节的水稻分蘖直接相关。
Carotenoids not only play important roles in light harvesting and photoprotection against excess light, but also serve as precursors for apocaroteniod hormones such as abscisic acid (ABA) and strigolactones (SLs). Although light- and ABA-associated phenotypes of the carotenoid biosynthesis mutants such as albino, leaf variegation and preharvest sprouting have been studied extensively, the SLs-related branching phenotype is rarely explored. Here we characterized four allelic rice mutants namedmit3, which exhibited moderately increased tiller number, semi-dwarfism and leaf variegation. Map-based cloning revealed thatMIT3encodes a carotenoid isomerase (CRTISO), the key enzyme catalyzing the conversion from prolycopene to all-trans-lycopene in carotenoid biosynthesis. Prolycopene was accumulated while all-trans-lycopene was barely detectable in the dark-grownmit3seedlings. Accordingly, content of lutein and β-carotene, the two most abundant carotenoids, was significantly reduced. Furthermore, content ofepi-5DS, a native SL, was significantly reduced inmit3.Exogenously applied GR24, a synthetic SL, could rescue the tillering phenotype ofmit3.Double mutant analysis ofmit3with the SLs biosynthesis mutantd17revealed thatMIT3controls tiller development upstream of the SLs biosynthesis pathway. Our results reveal that the tillering phenotype ofmit3is due to SL deficiency and directly link carotenoid deficiency with SL-regulated rice tillering.