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The enhancement of phototropin-induced phototropic curvature inarabidopsis occurs via a photoreversible phytochrome A-dependentmodulation of auxin responsiveness

机译:光合蛋白诱导的光合弯曲失禁的增强是通过植物生长素响应性的光可逆性植物色素A依赖性调节而发生的

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The induction of phototropism in etiolated (dark-grown) seedlings exposed to an unidirectional pulse or extended irradiation with low fluence rate blue light (BL) requires the action of the phototropin (nph1) BL receptor. Although cryptochromes and phytochromes are not required for phototropic induction, these photoreceptors do modulate the magnitude of curvature resulting from phototropin activation. Modulatory increases in the magnitude of phototropic curvature have been termed "enhancement." Here, we show that phototropic enhancement is primarily a phytochrome A (phyA)-dependent red/far-red-reversible low fluence response. This phyA-dependent response is genetically separable from the basal phototropin-dependent response, as demonstrated by its retention under extended irradiation conditions in the nph4 mutant background, which normally lacks the basal BL-induced response. It is interesting that the nph4 mutants fail to exhibit the basal phototropin-dependent and phyA-dependent enhancement responses under limiting light conditions. Given that NPH4 encodes a transcriptional activator, auxin response factor 7 (ARF7), we hypothesize that the ultimate target(s) of phyA action during the phototropic enhancement response is a rate-limiting ARF-containing transcriptional complex in which the constituent ARFs can vary in identity or activity depending upon the irradiation condition.
机译:在暴露于单向脉冲或低通量率蓝光(BL)的长时间照射下的黄化(深色)幼苗中,向光性的诱导需要光化蛋白(nph1)BL受体的作用。尽管光致诱导不需要隐色素和植物色素,但是这些感光体确实调节了由光养蛋白激活引起的曲率的大小。趋光性曲率的大小的调节增加被称为“增强”。在这里,我们表明光致增强主要是植物色素A(phyA)依赖的红色/远红色可逆的低通量响应。这种phyA依赖性反应在遗传上与基础光养蛋白依赖性反应是可分离的,这可以通过在延长的辐射条件下保留在nph4突变体背景下(通常缺乏基础BL诱导的反应)来证明。有趣的是,nph4突变体在有限的光照条件下无法表现出基础光养蛋白依赖性和phyA依赖性增强反应。假定NPH4编码一种转录激活因子生长素应答因子7(ARF7),我们假设在向光增强应答过程中phyA作用的最终目标是一个限速的含ARF的转录复合物,在该复合物中成分ARF可以变化身份或活动取决于照射条件。

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