Jaekel Robert, Klein Thomas
Institute for Genetics, University of Cologne, Zülpicherstrasse 47, 50674 Cologne, Germany.
Dev Cell. 2006 Nov;11(5):655-69. doi: 10.1016/j.devcel.2006.09.019.
Notch signaling is involved in many developmental and pathological processes, and its activity must be precisely controlled in order to prevent aberrant development and disease. We have previously shown that the tumor suppressor gene lethal (2) giant discs (lgd) is required to prevent ectopic activation of Notch in developmental processes in Drosophila. Here we show that lgd is required in all imaginal disc cells to suppress the activity of the Notch pathway. lgd encodes a member of a poorly characterized protein family present in all animals, which includes a member that is involved in an inheritable form of mental retardation in humans. Our analysis reveals that Lgd is required for endosomal trafficking of Notch and other proteins. In the absence of Lgd, Notch is activated in a ligand-independent manner in probably all imaginal disc cells in an endosomal compartment downstream of the block in hrs mutants.
Notch信号通路参与许多发育和病理过程,其活性必须得到精确控制,以防止发育异常和疾病。我们之前已经表明,肿瘤抑制基因致死(2)大圆盘(lgd)是果蝇发育过程中防止Notch异位激活所必需的。在这里我们表明,lgd在所有成虫盘细胞中都是抑制Notch信号通路活性所必需的。lgd编码一个存在于所有动物中的特征不明的蛋白质家族的成员,该家族包括一个与人类可遗传形式的智力迟钝有关的成员。我们的分析表明,Lgd是Notch和其他蛋白质内体运输所必需的。在没有Lgd的情况下,Notch可能在hrs突变体中阻断下游的内体区室中的所有成虫盘细胞中以配体非依赖的方式被激活。