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A Rice Brassinosteroid-Deficient Mutant, ebisu dwarf (d2), Is Caused by a Loss of Function of a New Member of Cytochrome P450

机译:水稻油菜素缺乏症的突变体,惠比寿矮(d2),是由细胞色素P450新成员的功能丧失引起的

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摘要

We characterized a rice dwarf mutant, ebisu dwarf (d2). It showed the pleiotropic abnormal phenotype similar to that of the rice brassinosteroid (BR)-insensitive mutant, d61. The dwarf phenotype of d2 was rescued by exogenous brassinolide treatment. The accumulation profile of BR intermediates in the d2 mutants confirmed that these plants are deficient in late BR biosynthesis. We cloned the D2 gene by map-based cloning. The D2 gene encoded a novel cytochrome P450 classified in CYP90D that is highly similar to the reported BR synthesis enzymes. Introduction of the wild D2 gene into d2-1 rescued the abnormal phenotype of the mutants. In feeding experiments, 3-dehydro-6-deoxoteasterone, 3-dehydroteasterone, and brassinolide effectively caused the lamina joints of the d2 plants to bend, whereas more upstream compounds did not cause bending. Based on these results, we conclude that D2/CYP90D2 catalyzes the steps from 6-deoxoteasterone to 3-dehydro-6-deoxoteasterone and from teasterone to 3-dehydroteasterone in the late BR biosynthesis pathway.
机译:我们表征了水稻矮化突变体惠比寿矮化(d2)。它显示了与水稻油菜素类固醇(BR)不敏感突变体d61相似的多效性异常表型。 d2的矮表型通过外源油菜素内酯处理得以挽救。 BR中间体在d2突变体中的积累情况证实,这些植物在BR的后期生物合成中缺乏。我们通过基于图的克隆克隆了D2基因。 D2基因编码一种分类为CYP90D的新型细胞色素P450,与报道的BR合成酶高度相似。将野生的D2基因导入d2-1可挽救突变体的异常表型。在补料实验中,3-dehydro-6-deoxoteasterone,3-dehydroteasterone和芸苔素内酯有效地导致d2植物的叶片关节弯曲,而更多的上游化合物则不会引起弯曲。根据这些结果,我们得出结论,D2 / CYP90D2催化了BR生物合成后期从6-脱氧孕甾酮到3-dehydro-6-脱氧孕甾酮以及从teasterone到3-dehydroteasterone的步骤。

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