The Class I basic helix–loop–helix (bHLH) proteins are highly conserved transcription factors that are ubiquitously expressed. A wealth of literature on Class I bHLH proteins has shown that these proteins must homodimerize or heterodimerize with tissue‐specific HLH proteins in order to bind DNA at E‐box consensus sequences to control tissue‐specific transcription. Due to its ubiquitous expression, Class I bHLH proteins are also extensively regulated posttranslationally, mostly through dimerization. Previously, we reported that in addition to its role in promoting neurogenesis, the Class I bHLH protein daughterless also functions in mature neurons to restrict axon branching and synapse number. Here, we show that part of the molecular logic that specifies how daughterless functions in neurogenesis is also conserved in neurons. We show that the Type V HLH protein extramacrochaetae (Emc) binds to and represses daughterless function by sequestering daughterless to the cytoplasm. This work provides initial insights into the mechanisms underlying the function of daughterless and Emc in neurons while providing a novel understanding of how Emc functions to restrict daughterless activity within the cell.

中文翻译：

---

宏观外寄生虫通过隔离无子daughter在神经元细胞质中来促进分支和钮扣数。

I类基本螺旋-环-螺旋（bHLH）蛋白是高度保守的转录因子，无处不在。关于I类bHLH蛋白的大量文献表明，这些蛋白必须与组织特异性HLH蛋白同二聚或异二聚体才能结合E-box共有序列上的DNA来控制组织特异性转录。由于其无处不在的表达，I类bHLH蛋白在翻译后也受到广泛的调节，主要是通过二聚作用。以前，我们报道过，除了其在促进神经发生中的作用外，I类bHLH蛋白无女儿还可以在成熟的神经元中发挥作用，以限制轴突的分支和突触数量。在这里，我们显示了分子逻辑的一部分，该分子逻辑指定了神经元中无子代功能的保守性。我们显示，V型HLH蛋白Extramacrochaetae（Emc）结合并通过隔离无子粒的细胞质抑制无子粒的功能。这项工作提供了对神经元中无子粒和Emc功能的基本机制的初步见解，同时提供了对Emc如何发挥作用来限制细胞内无子粒活动的新颖理解。