Hedgehog (Hh) signaling plays a central role in pattern formation by regulating transcription factor Cubitus interruptus (Ci). Previously, Roadkill (Rdx, also called HIB) was shown to inhibit Ci activity by two distinct mechanisms, depending on the Hh signal strength (Seong et al. 2010, PLoS One 5, e15365). In the anterior region abutting the anterior/posterior (A/P) boundary of the wing disk, where cells receive a strong Hh signal, Rdx blocks the nuclear entry of Ci-155. In contrast, in the region farther from the A/P boundary, where cells receive moderate levels of Hh, Rdx induces Ci-155 degradation in the nucleus. Here, we report that Suppressor of fused, Su(fu), causes the Rdx switch between mechanisms. A strong Hh signal induces rdx expression and suppresses su(fu) expression, whereas moderate levels of Hh induce moderate levels of rdx expression and high levels of su(fu) expression. Rdx blocks entry of Ci-155 into the nucleus in the absence of Su(fu) and Rdx induces the degradation of Ci-155 in the nucleus in the presence of a threshold level of Su(fu). Thus, the Su(fu)-induced switch between the dual actions of Rdx in response to the Hh signal strength plays a role in fine-tuning Hh signaling.
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机译：刺猬（Hh）信号通过调节转录因子Cubitus interruptus（Ci）在模式形成中起重要作用。以前，根据Hh信号强度，Roadkill（Rdx，也称为HIB）已显示出通过两种不同的机制抑制Ci的活性（Seong等，2010，PLoS One 5，e15365）。在与翼片的前/后（A / P）边界邻接的前部区域（细胞在其中接收强Hh信号），Rdx阻止了Ci-155的核进入。相反，在距离A / P边界较远的区域（该区域细胞接受中等水平的Hh），Rdx诱导细胞核中的Ci-155降解。在这里，我们报告说，融合的抑制器Su（fu）导致机制之间的Rdx切换。强Hh信号诱导rdx表达并抑制su（fu）表达，而中等水平的Hh诱导中等水平的rdx表达和高水平的su（fu）表达。在不存在Su（fu）的情况下，Rdx阻止Ci-155进入细胞核，在存在Su（fu）阈值水平的情况下，Rdx诱导在细胞核中Ci-155降解。因此，Su（fu）响应于Hh信号强度在Rdx的双重作用之间引起的切换在微调Hh信号中起着作用。
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