Spenito and Split ends act redundantly to promote Wingless signaling
Spenito and Split ends act redundantly to promote Wingless signaling
复制标题
DOI：
10.1016/j.ydbio.2007.11.023
复制
发表时间：
2008-02-01
影响因子：
2.7
通讯作者：
Cadigan, Ken M.
中科院分区：
文献类型：
--
作者：
Chang, Jinhee L.;Lin, Hua V.;Cadigan, Ken M.
无翅（Wg）/Wnt信号传导通过促进Armadillo/β-连环蛋白与Wg调节增强子（WRE）上的TCF的缔合来指导动物发育期间的各种细胞过程。分裂末端（Spen），一种含有RNA识别基序（RRM）和SPOC结构域的核蛋白，是几种果蝇组织中最佳Wg信号传导所必需的。在这份报告中，我们证明了Spenito（Nito），唯一的其他苍蝇蛋白含有RRM和SPOC结构域，与Spen一起积极调节Wg信号。用spen RNAi观察到的Wg信号传导中的部分缺陷通过同时敲低nito而增强，而通过在翅成虫盘中表达nito而拯救。在细胞培养中，两种因子的耗尽导致几种Wg靶标的激活比单独的spen或nito的RNAi更大的缺陷。这些核蛋白不是犰狳稳定或募集TCF和犰狳到WRE所必需的。Wg靶基因激活的损失，在细胞耗尽的spen和nito是不依赖于转录抑制Yan或抑制无毛，两个先前确定的Spen的目标。我们建议，Spen和Nito作用于TCF/Armadillo的冗余下游，以激活许多Wg转录靶点。(C)2007爱思唯尔公司All rights reserved.
Wingless (Wg)/Wnt signaling directs a variety of cellular processes during animal development by promoting the association of Armadillo/beta-catenin with TCFs on Wg-regulated enhancers (WREs). Split ends (Spen), a nuclear protein containing RNA recognition motifs (RRMs) and a SPOC domain, is required for optimal Wg signaling in several fly tissues. In this report, we demonstrate that Spenito (Nito), the only other fly protein containing RRMs and a SPOC domain, acts together with Spen to positively regulate Wg signaling. The partial defect in Wg signaling observed with spen RNAi was enhanced by simultaneous knockdown of nito while it was rescued by expression of nito in wing imaginal discs. In cell culture, depletion of both factors causes a greater defect in the activation of several Wg targets than RNAi of either spen or nito alone. These nuclear proteins are not required for Armadillo stabilization or the recruitment of TCF and Armadillo to a WRE. Loss of Wg target gene activation in cells depleted for spen and nito was not dependent on the transcriptional repressor Yan or Suppressor of Hairless, two previously identified targets of Spen. We propose that Spen and Nito act redundantly downstream of TCF/Armadillo to activate many Wg transcriptional targets. (C) 2007 Elsevier Inc. All rights reserved.