The Drosophila secreted protein argos regulates signal transduction in the Ras/MAPK pathway
The Drosophila secreted protein argos regulates signal transduction in the Ras/MAPK pathway
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DOI：
10.1006/dbio.1996.0194
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发表时间：
1996-08-25
影响因子：
2.7
通讯作者：
Okano, H
中科院分区：
文献类型：
--
作者：
Sawamoto, K;Okabe, M;Okano, H
果蝇基因编码一种具有EGF基序的分泌蛋白，该蛋白在多种发育过程中作为细胞分化的抑制剂。为了研究Argos调控的细胞通路，我们筛选了可以改变Argos过表达引起的表型的突变。我们发现argos过表达对眼睛和翅膀静脉发育的影响被MAPKK/D-MEK基因（Dsor1/ D-MEK）和MAPK/ERK-A基因（rolled）的功能获得突变抑制，而被Star的功能缺失突变增强。Ras/MAPK信号级联组件的功能丧失突变是argos无效突变引起的表型的主要抑制因子。功能缺失的argos突变增强了由Son of sevenless和Dsor1的功能获得等位基因引起的R7神经元的过量产生。相反，argos的过表达抑制了由高水平MAPK/ERK-A活性引起的额外R7细胞的形成。sev的表型；Argos双突变体揭示了sev对Argos的上位性。这些结果提供了Argos负调控Ras/MAPK级联信号转导事件的证据。(C) 1996学术出版社，Inc.
The Drosophila argos gene encodes a secreted protein with an EGF motif which acts as an inhibitor of cellular differentiation in multiple developmental processes. To investigate the cellular pathways regulated by Argos, we screened for mutations which could modify the phenotype caused by overexpression of argos. We show that the effects of argos overexpression on the eye and wing vein development are suppressed by gain-of-function mutations of the MAPKK/D-MEK gene (Dsor1/D-mek) and the MAPK/ERK-A gene (rolled) and were enhanced by loss-of-function mutations of Star. Loss-of-function mutations in components of the Ras/MAPK signaling cascade act as dominant suppressors of the phenotype caused by the argos null mutation. A loss-of-function argos mutation enhanced the overproduction of R7 neurons caused by gain-of-function alleles of Son of sevenless and Dsor1. Conversely, overexpression of argos inhibited formation of the extra R7 cells that was caused by high-level MAPK/ERK-A activity. A phenotype of the sev; argos double mutants revealed that sev is epistatic to argos. These results provide evidence that Argos negatively regulates signal transduction events in the Ras/MAPK cascade. (C) 1996 Academic Press, Inc.