Ye Y, Fortini M E
Department of Genetics, University of Pennsylvania School of Medicine, Stellar-Chance Laboratories 709C, Philadelphia 19104, USA.
Mech Dev. 1998 Dec;79(1-2):199-211. doi: 10.1016/s0925-4773(98)00169-5.
Mutant Presenilin proteins cause early-onset familial Alzheimer's disease in humans and Caenorhabditis elegans Presenilins may facilitate Notch receptor signaling. We have isolated a Drosophila Presenilin homologue and determined the spatial and temporal distribution of the encoded protein as well as its localization relative to the fly Notch protein. In contrast to previous mRNA in situ studies, we find that Presenilin is widely expressed throughout oogenesis, embryogenesis, and imaginal development, and generally accumulates at comparable levels in neuronal and nonneuronal tissues. Double immunolabeling with Notch antibodies revealed that Presenilin and Notch are coexpressed in many tissues throughout Drosophila development and display partially overlapping subcellular localizations, supporting a possible functional link between Presenilin and Notch.
突变型早老素蛋白会导致人类和秀丽隐杆线虫出现早发性家族性阿尔茨海默病。早老素可能会促进Notch受体信号传导。我们分离出了一种果蝇早老素同源物,并确定了编码蛋白的时空分布及其相对于果蝇Notch蛋白的定位。与之前的mRNA原位研究不同,我们发现早老素在卵子发生、胚胎发生和成虫发育过程中广泛表达,并且在神经元和非神经元组织中的积累水平通常相当。用Notch抗体进行双重免疫标记显示,在果蝇发育的许多组织中,早老素和Notch共同表达,并且显示出部分重叠的亚细胞定位,这支持了早老素和Notch之间可能存在功能联系。