The basic helix-loop-helix transcription factor PIF5 acts on ethylene biosynthesis and phytochrome signaling by distinct mechanisms
The basic helix-loop-helix transcription factor PIF5 acts on ethylene biosynthesis and phytochrome signaling by distinct mechanisms
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DOI：
10.1105/tpc.107.051508
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发表时间：
2007-12-01
期刊：
影响因子：
11.6
通讯作者：
Quail, Peter H.
中科院分区：
文献类型：
--
作者：
Khanna, Rajnish;Shen, Yu;Quail, Peter H.
光敏色素相互作用因子5（PIF 5）是一种碱性螺旋-环-螺旋转录因子，与光敏色素B（phyB）的光活化形式特异性相互作用。在这里，我们报告说，黑暗生长的拟南芥幼苗过度表达PIF 5（PIF 5-OX）表现出夸张的顶端钩和短下胚轴，让人想起乙烯水平升高诱导的三重反应，而pif 5突变体不能保持紧钩像野生型幼苗。银离子，一种乙烯受体阻断剂，挽救了三重反应表型，我们表明，PIF 5-OX幼苗表达增强水平的关键乙烯生物合成酶，并产生升高的乙烯水平。PIF 5-OX幼苗暴露于延长的连续红光（Rc）相对于黑暗对照促进下胚轴伸长，这是野生型幼苗显示的Rc施加的下胚轴抑制的倒数。与这种PIF 5-OX对Rc的低敏感性相反，pif 5突变体幼苗相对于野生型幼苗是超敏感的。我们发现，这种对比是由于phyB蛋白水平在长期RC的相互变化。与野生型幼苗相比，PIF 5-OX幼苗Rc中的phyB（和phyC）水平降低，而pif 5突变体Rc中的phyB（和phyC）水平升高。过表达体中的phyB降解依赖于PIF 5中的功能性phyB结合基序，并涉及26 S蛋白酶体途径。因此，我们的数据表明，过度表达的PIF 5导致乙烯水平改变，这促进了黑暗中的三重响应，而在光下，光活化的phyB与PIF 5的相互作用导致光感受器蛋白的降解。有证据表明，内源性PIF 5负调节phyB施加的下胚轴抑制延长Rc通过减少光感受器丰度，从而感光能力，而不是作为一个信号中间体。
PHYTOCHROME-INTERACTING FACTOR5 (PIF5), a basic helix-loop-helix transcription factor, interacts specifically with the photoactivated form of phytochrome B ( phyB). Here, we report that dark-grown Arabidopsis thaliana seedlings over-expressing PIF5 (PIF5-OX) exhibit exaggerated apical hooks and short hypocotyls, reminiscent of the triple response induced by elevated ethylene levels, whereas pif5 mutants fail to maintain tight hooks like those of wild-type seedlings. Silver ions, an ethylene receptor blocker, rescued the triple-response phenotype, and we show that PIF5-OX seedlings express enhanced levels of key ethylene biosynthesis enzymes and produce elevated ethylene levels. Exposure of PIF5-OX seedlings to prolonged continuous red light (Rc) promotes hypocotyl elongation relative to dark controls, the reciprocal of the Rc-imposed hypocotyl inhibition displayed by wild-type seedlings. In contrast with this PIF5-OX hyposensitivity to Rc, pif5 mutant seedlings are hypersensitive relative to wild-type seedlings. We show that this contrast is due to reciprocal changes in phyB protein levels in prolonged Rc. Compared with wild-type seedlings, PIF5-OX seedlings have reduced, whereas pif5 mutants have increased, phyB (and phyC) levels in Rc. The phyB degradation in the overexpressors depends on a functional phyB binding motif in PIF5 and involves the 26S proteasome pathway. Our data thus indicate that overexpressed PIF5 causes altered ethylene levels, which promote the triple response in darkness, whereas in the light, the interaction of photoactivated phyB with PIF5 causes degradation of the photoreceptor protein. The evidence suggests that endogenous PIF5 negatively regulates phyB-imposed hypocotyl inhibition in prolonged Rc by reducing photoreceptor abundance, and thereby photosensory capacity, rather than functioning as a signaling intermediate.