Su(fu) switches Rdx functions to fine-tune hedgehog signaling in the Drosophila wing disk

Su(fu) switches Rdx functions to fine-tune hedgehog signaling in the Drosophila wing disk
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Su(fu)切换Rdx功能以微调果蝇翼盘中的hedgehog信号

DOI:
10.1111/gtc.12018
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发表时间:
2013
期刊:
影响因子:
2.1
通讯作者:
Seong KH & Ishii S
Seong KH & Ishii S
中科院分区:
生物学4区
文献类型:
--
作者:
Kondo H;Kusaka S;Yoshinaga A;Uchio E;Tawara A;Tahira T;松本経;大塚俊之;Seong KH & Ishii S

文献摘要

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Hedgehog(Hh)信号通过调节转录因子Cubitus interruptus(Ci)在模式形成中起核心作用。先前,路杀(Rdx,也称为HIB)显示通过两种不同的机制抑制Ci活性,这取决于Hh信号强度(Seonget al. 2010,PLoS One5,e15365)。在与翼盘的前/后(A/P)边界相邻的前部区域,细胞接收到强烈的Hh信号,Rdx阻断了Ci-155的核进入。相反,在远离A/P边界的区域,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,抑制剂的融合,苏(fu),导致机制之间的Rdx开关。强Hh信号诱导rdx表达和抑制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阻断Ci-155进入细胞核,并且在存在阈值水平的Su(fu)的情况下,Rdx诱导细胞核中Ci-155的降解。因此,Su(fu)诱导的Rdx响应Hh信号强度的双重作用之间的转换在微调Hh信号中起作用。
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 (Seonget al. 2010,PLoS One5, 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 inducesrdxexpression and suppressessu(fu)expression, whereas moderate levels of Hh induce moderate levels ofrdxexpression and high levels ofsu(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.