Plants detect proximity of competitors through reduction in the ratio between red and far-red light that triggers the shade avoidance syndrome, inducing responses such as accelerated shoot elongation and early flowering. Shade avoidance is regulated by PHYTOCHROME INTERACTING FACTORs, a group of basic helix-loop-helix (bHLH) transcription factors. Another (b)HLH protein, KIDARI (KDR), which is non-DNA-binding, was identified in de-etiolation studies and proposed to interact with LONG HYPOCOTYL IN FAR-RED1 (HFR1), a (b)HLH protein that inhibits shade avoidance. Here, we established roles of KDR in regulating shade avoidance in Arabidopsis (Arabidopsis thaliana) and investigated how KDR regulates the shade avoidance network. We showed that KDR is a positive regulator of shade avoidance and interacts with several negative growth regulators. We identified KDR interactors using a combination of yeast two-hybrid screening and dedicated confirmations with bimolecular fluorescence complementation. We demonstrated that KDR is translocated primarily to the nucleus when coexpressed with these interactors. A genetic approach confirmed that several of these interactions play a functional role in shade avoidance; however, we propose that KDR does not interact with HFR1 to regulate shade avoidance. Based on these observations, we propose that shade avoidance is regulated by a three-layered gas-and-brake mechanism of bHLH protein interactions, adding a layer of complexity to what was previously known.

植物通过减少触发遮阴综合症的红光和远红光之比来检测竞争对手的接近程度，从而诱导诸如加快枝伸长和早开花等反应。避光受植物染色体相互作用因子（PIF）调节，PIF是一组bHLH转录因子。另一种（b）HLH蛋白KIDARI（KDR）是非DNA结合的，已在去甲化研究中得到鉴定，并建议与FAR-RED 1（HFR1）中的长羟基油菜碱相互作用，这是一种（b）HLH蛋白，禁止避光。在这里，我们建立了KDR在调节拟南芥中避光的作用，并研究了KDR如何调控避光网络。我们表明，KDR是避光的正调节剂，并与几个负增长调节剂相互作用。我们使用酵母双杂交筛选和专门的确认与双分子荧光互补相结合，确定了KDR相互作用子。我们证明了与这些相互作用分子共表达时，KDR主要易位至细胞核。遗传方法证实了其中的几种相互作用在避光方面发挥了作用。但是，我们建议KDR不与HFR1相互作用来调节避光。基于这些观察，我们建议避光是通过bHLH蛋白相互作用的三层气体和制动机制来调节的，从而为先前已知的问题增加了一层复杂性。我们证明了与这些相互作用分子共表达时，KDR主要易位至细胞核。遗传方法证实了其中的几种相互作用在避光方面发挥了作用。但是，我们建议KDR不与HFR1相互作用来调节避光。基于这些观察，我们建议避光是通过bHLH蛋白相互作用的三层气体和制动机制来调节的，从而为先前已知的问题增加了一层复杂性。我们证明了与这些相互作用分子共表达时，KDR主要易位至细胞核。遗传方法证实了其中的几种相互作用在避光方面发挥了作用。但是，我们建议KDR不与HFR1相互作用来调节避光。基于这些观察，我们建议避光是通过bHLH蛋白相互作用的三层气体和制动机制来调节的，从而为先前已知的问题增加了一层复杂性。