Gibberellins modulate light signaling pathways to prevent Arabidopsis seedling de-etiolation in darkness
Gibberellins modulate light signaling pathways to prevent Arabidopsis seedling de-etiolation in darkness
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DOI：
10.1111/j.1365-313x.2007.03346.x
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发表时间：
2008-01-01
期刊：
影响因子：
7.2
通讯作者：
Blazquez, Miguel A.
中科院分区：
文献类型：
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作者：
Alabadi, David;Gallego-Bartolome, Javier;Blazquez, Miguel A.
在许多植物中，光形态建成是种子萌发后的默认发育程序，并提供了允许适应光的关键特征。如果在无光条件下萌发，该程序被积极抑制，其机制依赖于由COP1编码的拟南芥中E3泛素连接酶的活性(BAR同源基因1下的BAR NSTITUTIVE(P)下的(CO)，它诱导光调控发育所需的转录因子的蛋白降解，例如BAR POCOTYL 5(BAR OMOLOG下的POCOTYL 5(H)下的HY5(Long(HY))和BAR OMOLOG下的BAR POCOTYL 5(H)下的HYH)，以及促进形态发生的转录因子的稳定，例如BAR(I)下的PIF3(P)。缺乏赤霉素(GA)合成或信号的幼苗在黑暗中生长时表现出去黄化的表型，相当于Cop1突变体的表型，这表明光形态建成和茎形态建成之间的转换也受到激素的控制。在这里，我们提供了GA和COP1介导的途径之间存在串扰的证据，并将HY5和PIF家族确定为调控网络的节点。这种相互作用通过不同的分子机制发生，基于观察到GA信号调节HY5的蛋白质稳定性和PIF3的活性。
In many plants, photomorphogenesis is the default developmental program after seed germination, and provides the key features that allow adaptation to light. This program is actively repressed if germination occurs in the absence of light, through a mechanism dependent on the E3 ubiquitin ligase activity that is encoded in Arabidopsis by COP1 ((CO) under bar NSTITUTIVE (P) under bar HOTOMORPHOGENIC 1), which induces proteolytic degradation of transcription factors necessary for light-regulated development, such as HY5 (LONG (HY) under bar POCOTYL 5) and HYH (LONG (HY) under bar POCOTYL 5 (H) under bar OMOLOG), and stabilization of transcription factors that promote skotomorphogenesis, such as PIF3 ((P) under bar HYTOCHROME (I) under bar NTERACTING (F) under bar ACTOR 3). Seedlings deficient in gibberellin (GA) synthesis or signaling display a de-etiolated phenotype when grown in darkness, equivalent to the phenotype of cop1 mutants, which indicates that the switch between photo- and skotomorphogenesis is also under hormonal control. Here we provide evidence for the existence of crosstalk between GA and the COP1-mediated pathway, and identify HY5 and the PIF family as nodes of a regulatory network. This interaction occurs through distinct molecular mechanisms, based on the observation that GA signaling regulates protein stability of HY5, and the activity of PIF3.