Phytochrome interacting factors 4 and 5 redundantly limit seedling de-etiolation in continuous far-red light
Phytochrome interacting factors 4 and 5 redundantly limit seedling de-etiolation in continuous far-red light
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DOI：
10.1111/j.1365-313x.2009.03971.x
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发表时间：
2009-11-01
期刊：
影响因子：
7.2
通讯作者：
Fankhauser, Christian
中科院分区：
文献类型：
--
作者：
Lorrain, Severine;Trevisan, Martine;Fankhauser, Christian
植物色素是红光/远红光光感受器，可调节植物中的众多发育过程。其中，植物色素A（phyA）对于在连续远红光（FR）下使幼苗去黄化至关重要，这种条件模拟了茂密树冠下的环境。phyA突变体植物在植被茂密的荫蔽处萌发时的高死亡率证明了这种反应的生态相关性。phyA信号传导涉及光感受器与植物色素相互作用因子PIF1和PIF3（bHLH转录因子家族成员）的直接相互作用。在此我们研究了PIF4和PIF5在phyA信号传导中的作用，发现它们在远红光下冗余地控制去黄化。pif4 pif5双突变体对低通量率的远红光高度敏感。这种表型依赖于phyA对远红光的感知，但不依赖于phyA水平的改变。我们的微阵列分析表明，PIF4和PIF5是一种抑制机制的一部分，该机制在黑暗中抑制一些光响应基因的表达，并且它们对于光下几个生长相关基因的充分表达也是必需的。与PIF1和PIF3不同，PIF4和PIF5不会因远红光而降解，这表明它们是通过不同的机制受光调节的。我们的遗传分析表明，这是通过密切相关的bHLH转录因子HFR1（远红光下长下胚轴）对这些PIF的隔离来实现的。
P>Phytochromes are red/far-red photosensors that regulate numerous developmental programs in plants. Among them, phytochrome A (phyA) is essential to enable seedling de-etiolation under continuous far-red (FR) light, a condition that mimics the environment under a dense canopy. The ecological relevance of this response is demonstrated by the high mortality rate of phyA mutant plants that germinate in deep vegetational shade. phyA signaling involves direct interaction of the photoreceptor with phytochrome-interacting factors PIF1 and PIF3, members of the bHLH transcription factor family. Here we investigated the involvement of PIF4 and PIF5 in phyA signaling, and found that they redundantly control de-etiolation in FR light. The pif4 pif5 double mutant is hypersensitive to low fluence rates of FR light. This phenotype is dependent on FR light perception by phyA, but does not rely on alterations in the phyA level. Our microarray analysis shows that PIF4 and PIF5 are part of an inhibitory mechanism that represses the expression of some light-responsive genes in the dark, and that they are also needed for full expression of several growth-related genes in the light. Unlike PIF1 and PIF3, PIF4 and PIF5 are not degraded in response to FR light, indicating that they are light-regulated by a different mechanism. Our genetic analysis suggests that this is achieved through sequestration of these PIFs by the closely related bHLH transcription factor HFR1 (long hypocotyl in FR light).