The shade avoidance syndrome in Arabidopsis: a fundamental role for atypical basic helix-loop-helix proteins as transcriptional cofactors
The shade avoidance syndrome in Arabidopsis: a fundamental role for atypical basic helix-loop-helix proteins as transcriptional cofactors
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DOI：
10.1111/j.1365-313x.2011.04485.x
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发表时间：
2011-04-01
期刊：
影响因子：
7.2
通讯作者：
Martinez-Garcia, Jaime F.
中科院分区：
文献类型：
--
作者：
Galstyan, Anahit;Cifuentes-Esquivel, Nicolas;Martinez-Garcia, Jaime F.
P>避荫综合症（SAS）是指一组旨在预测潜在竞争者最终遮荫的植物反应。 SAS 在感知到附近植被后启动，因为入射光的红光与远红光比率 (R:FR) 有所降低。光敏色素感知到低 R:FR 光，引发基因表达的巨大变化，最终导致幼苗的下胚轴伸长增加，从而使竞争者过度生长。这种反应受到 PHYTOCHROME RAPIDLY REGULATED 1 (PAR1)、PAR2 和 LONG HYPOCOTYL IN FR 1 (HFR1) 等基因的抑制，这些基因是由低 R:FR 转录诱导的。尽管 PAR1/PAR2 和 HFR1 蛋白属于不同组的碱性螺旋-环-螺旋 (bHLH) 转录调节因子，但它们都缺乏与靶基因启动子中的 E-box 和 G-box 基序结合所需的典型基本结构域。通过过表达 PAR1 和 HFR1 的衍生物，我们表明这些蛋白实际上是转录辅助因子，不需要结合 DNA 来直接调节转录。我们得出的结论是，涉及 PAR1 和 HFR1 的 HLH 结构域的蛋白质-蛋白质相互作用是这些蛋白质调节基因表达的机制的一个基本方面，最有可能是通过与真正的转录因子相互作用，这些转录因子确实与靶基因结合并最终释放观察到的 SAS 反应。
P>The shade avoidance syndrome (SAS) refers to a set of plant responses aimed at anticipating eventual shading by potential competitors. The SAS is initiated after perception of nearby vegetation as a reduction in the red to far-red ratio (R:FR) of the incoming light. Low R:FR light is perceived by the phytochromes, triggering dramatic changes in gene expression that, in seedlings, eventually result in an increased hypocotyl elongation to overgrow competitors. This response is inhibited by genes such as PHYTOCHROME RAPIDLY REGULATED 1 (PAR1), PAR2 and LONG HYPOCOTYL IN FR 1 (HFR1), which are transcriptionally induced by low R:FR. Although PAR1/PAR2 and HFR1 proteins belong to different groups of basic helix-loop-helix (bHLH) transcriptional regulators, they all lack a typical basic domain required for binding to E-box and G-box motifs in the promoter of target genes. By overexpressing derivatives of PAR1 and HFR1 we show that these proteins are actually transcriptional cofactors that do not need to bind DNA to directly regulate transcription. We conclude that protein-protein interactions involving the HLH domain of PAR1 and HFR1 are a fundamental aspect of the mechanism by which these proteins regulate gene expression, most likely through interaction with true transcription factors that do bind to the target genes and eventually unleash the observed SAS responses.