Lu Q, Soria J P, Wood J G
Department of Anatomy and Cell Biology, Emory University School of Medicine, Atlanta, Georgia 30322.
J Neurosci Res. 1993 Jul 1;35(4):439-44. doi: 10.1002/jnr.490350411.
Abnormally phosphorylated tau protein is a major component of the cytoskeletal pathology of Alzheimer's disease (AD) found in the neurofibrillary tangle (NFT) and neuritic plaque (NP). Identification of the kinase responsible for this phosphorylation has been difficult. In the test tube, several proline-directed kinases, particularly mitogen-activated protein (MAP) and cdc2 kinase, phosphorylate tau on sites that appear to mimic the abnormally phosphorylated sites in AD. Important unanswered issues include: 1) whether this phosphorylation event occurs in the tightly regulated environment of a living cell; 2) whether this phosphorylation of tau affects its functional properties; and 3) what is the subcellular relationship of proline-directed kinases and tau. We show here that tau can be phosphorylated in cultured hippocampal neurons by the MAP kinase p44mpk, and phosphorylation of tau compromises its functional ability to assemble microtubules. We show further that MAP kinase copurifies with microtubule fractions where it is tyrosine phosphorylated and presumably active. These studies address and raise several important issues regarding the regulation of tau phosphorylation in normal and AD brain.
异常磷酸化的tau蛋白是阿尔茨海默病(AD)细胞骨架病理学的主要成分,见于神经原纤维缠结(NFT)和神经炎斑块(NP)中。确定负责这种磷酸化的激酶一直很困难。在试管中,几种脯氨酸定向激酶,特别是丝裂原活化蛋白(MAP)激酶和细胞分裂周期蛋白2(cdc2)激酶,可在似乎模拟AD中异常磷酸化位点的位置上使tau磷酸化。重要的未解决问题包括:1)这种磷酸化事件是否发生在活细胞的严格调控环境中;2)tau的这种磷酸化是否会影响其功能特性;3)脯氨酸定向激酶与tau的亚细胞关系是什么。我们在此表明,tau可在培养的海马神经元中被MAP激酶p44mpk磷酸化,且tau的磷酸化会损害其组装微管的功能能力。我们进一步表明,MAP激酶与微管部分共纯化,在那里它被酪氨酸磷酸化且可能具有活性。这些研究探讨并提出了一些关于正常和AD脑内tau磷酸化调节的重要问题。