Characterisation of Upd2, a Drosophila JAK/STAT pathway ligand
Characterisation of Upd2, a Drosophila JAK/STAT pathway ligand
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DOI：
10.1016/j.ydbio.2005.09.040
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发表时间：
2005-12-15
影响因子：
2.7
通讯作者：
Zeidler, MP
中科院分区：
文献类型：
--
作者：
Hombría, JCG;Brown, S;Zeidler, MP
激活JAK/STAT通路的配体的表征有可能揭示这一重要信号转导级联的一个相对知之甚少的方面。在这里，我们描述了我们的分析，唯一的无脊椎动物JAK/STAT途径配体确定的日期，果蝇未配对的家庭。我们表明，upd 2的表达模式基本相同的upd，并证明该区域编码的蛋白质激活JAK/STAT信号通路。突变分析表明，在已知需要JAK/STAT信号传导的多种组织中可以观察到相互半冗余。为了更好地研究这些配体的体内功能，我们开发了一种基于天然JAK/STAT通路应答增强子的报告基因，并表明异位upd 2表达可以有效地激活JAK/STAT通路。而Upd和Upd 2都是分泌型JAK/STAT途径激动剂。组织培养测定显示Upd和Upd 2的信号序列赋予不同的性质，Upd主要与细胞外基质相关，而Upd 2分泌到培养基中。不同的生物物理特性确定的upd样分子的影响，其功能在体内，并增加了母亲方面，我们的理解细胞因子信号在果蝇。(c)2005年爱思唯尔公司All rights reserved.
The characterisation of ligands that activate the JAK/STAT pathway has the potential to throw light onto a comparatively poorly understood aspect of this important signal transduction cascade. Here, we describe our analysis of the only invertebrate JAK/STAT pathway ligands identified to date, the Drosophila unpaired-like family. We show that upd2 is expressed in a pattern essentially identical to that of upd and demonstrate that the proteins encoded by this region activate JAK/STAT pathway signalling. Mutational analysis demonstrates a mutual semi-redundancy that can be visualised in multiple tissues known to require JAK/STAT signalling. In order to better characterise the in vivo function of these ligands, we developed a reporter based on a natural JAK/STAT pathway responsive enhancer and show that ectopic upd2 expression can effectively activate the JAK/STAT pathway. While both Upd and Upd2 are secreted JAK/STAT pathway agonists. tissue culture assays show that the signal-sequences of Upd and Upd2 confer distinct properties, with Upd associated primarily with the extracellular matrix and Upd2 secreted into the media. The differing biophysical characteristics identified for Upd-like molecules have implications for their Function in vivo and adds mother aspect to our understanding of cytokine signalling in Drosophila. (c) 2005 Elsevier Inc. All rights reserved.