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PIN 生长素外排载体对于脉冲诱导而非连续光照诱导的拟南芥光向性是必要的。

PIN auxin efflux carriers are necessary for pulse-induced but not continuous light-induced phototropism in Arabidopsis.

机构信息

Graduate School of Science and Technology, Niigata University, 8050 Ikarashi 2-no-cho, Nishi-ku, Niigata 950-2181, Japan.

出版信息

Plant Physiol. 2012 Oct;160(2):763-76. doi: 10.1104/pp.112.202432. Epub 2012 Jul 27.

Abstract

Auxin efflux carrier PIN-FORMED (PIN) proteins are thought to have central roles in regulating asymmetrical auxin translocation during tropic responses, including gravitropism and phototropism, in plants. Although PIN3 is known to be involved in phototropism in Arabidopsis (Arabidopsis thaliana), no severe defects of phototropism in any of the pin mutants have been reported. We show here that the pulse-induced, first positive phototropism is impaired partially in pin1, pin3, and pin7 single mutants, and severely in triple mutants. In contrast, such impairment was not observed in continuous-light-induced second positive phototropism. Analysis with an auxin-reporter gene demonstrated that PIN3-mediated auxin gradients participate in pulse-induced phototropism but not in continuous-light-induced phototropism. Similar functional separation was also applicable to PINOID, a regulator of PIN localization. Our results strongly suggest the existence of functionally distinct mechanisms i.e. a PIN-dependent mechanism in which transient stimulation is sufficient to induce phototropism, and a PIN-independent mechanism that requires continuous stimulation and does not operate in the former phototropism process. Although a previous study has proposed that blue-light photoreceptors, the phototropins, control PIN localization through the transcriptional down-regulation of PINOID, we could not detect this blue-light-dependent down-regulation event, suggesting that other as yet unknown mechanisms are involved in phototropin-mediated phototropic responses.

摘要

生长素外排载体 PIN 形成蛋白(PIN)被认为在调节植物向性反应中的不对称生长素转运中起核心作用,包括向重性和向光性。虽然已知 PIN3 参与拟南芥(Arabidopsis thaliana)的向光性,但在任何 pin 突变体中都没有报道过严重的向光性缺陷。我们在这里表明,在 pin1、pin3 和 pin7 单突变体中,脉冲诱导的第一正向向光性部分受损,而在三突变体中则严重受损。相比之下,在连续光照诱导的第二正向向光性中没有观察到这种损伤。利用生长素报告基因分析表明,PIN3 介导的生长素梯度参与脉冲诱导的向光性,但不参与连续光照诱导的向光性。PIN 定位调节剂 PINOID 也存在类似的功能分离。我们的研究结果强烈表明存在功能上不同的机制,即一个依赖 PIN 的机制,其中瞬时刺激足以诱导向光性,以及一个不依赖 PIN 的机制,它需要连续刺激,并且在以前的向光性过程中不起作用。尽管之前的研究提出蓝光受体光受体通过 PINOID 的转录下调来控制 PIN 的定位,但我们未能检测到这种蓝光依赖性下调事件,这表明蓝光介导的向光性反应涉及其他未知的机制。

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