COMPLEMENTARY DISTRIBUTION OF TAU PROTEINS IN DIFFERENT PHOSPHORYLATION STATES WITHIN GROWING AXONS

被引:22
作者
REBHAN, M [1 ]
VACUN, G [1 ]
ROSNER, H [1 ]
机构
[1] UNIV HOHENHEIM,INST ZOOL 220,D-70593 STUTTGART,GERMANY
关键词
TAU PROTEINS; PHOSPHORYLATION; ALZHEIMERS DISEASE; DEVELOPMENT; NEURITOGENESIS; COMPARTMENTATION; AXONAL GROWTH;
D O I
10.1097/00001756-199502000-00006
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
MICROTUBULE-associated tau proteins are hyperphosphorylated in brains from patients with Alzheimer's disease compared with normal adult human brain. At least some of the phosphorylated residues are also transiently phosphorylated in juvenile brain, but not in more mature stages. Using the monoclonal anti-tau antibodies TAU-1 and AT8, we found in cultured embryonic chicken and rat neurones a clear differential distribution of immunostaining within growing axons. Tau proteins that are phosphorylated at Ser202 (recognized by AT8) appear to be concentrated in the axonal portion that is close to the cell body and they decrease in proximal-distal direction. In contrast, tau proteins carrying an epitope that contains dephospho-Ser202 (recognized by TAU-1) are enriched in the distal axon and the growth cone. In colchicine-treated, growth-inhibited neurones there was an intense TAU-1 staining of the perikarya, but no longer any staining by AT8.
引用
收藏
页码:429 / 432
页数:4
相关论文
共 22 条
[1]   THE SWITCH OF TAU-PROTEIN TO AN ALZHEIMER-LIKE STATE INCLUDES THE PHOSPHORYLATION OF 2 SERINE PROLINE MOTIFS UPSTREAM OF THE MICROTUBULE BINDING REGION [J].
BIERNAT, J ;
MANDELKOW, EM ;
SCHROTER, C ;
LICHTENBERGKRAAG, B ;
STEINER, B ;
BERLING, B ;
MEYER, H ;
MERCKEN, M ;
VANDERMEEREN, A ;
GOEDERT, M ;
MANDELKOW, E .
EMBO JOURNAL, 1992, 11 (04) :1593-1597
[2]  
BINDER LI, 1985, J CELL BIOL, V101, P1371, DOI 10.1083/jcb.101.4.1371
[3]   A SEQUENCE OF CYTOSKELETON CHANGES RELATED TO THE FORMATION OF NEUROFIBRILLARY TANGLES AND NEUROPIL THREADS [J].
BRAAK, E ;
BRAAK, H ;
MANDELKOW, EM .
ACTA NEUROPATHOLOGICA, 1994, 87 (06) :554-567
[4]  
BRAMBLETT GT, 1993, NEURON, V10, P1080
[5]   DEVELOPMENTAL-CHANGES IN TAU-PHOSPHORYLATION - FETAL-TAU IS TRANSIENTLY PHOSPHORYLATED IN A MANNER SIMILAR TO PAIRED HELICAL FILAMENT-TAU CHARACTERISTIC OF ALZHEIMERS-DISEASE [J].
BRION, JP ;
SMITH, C ;
COUCK, AM ;
GALLO, JM ;
ANDERTON, BH .
JOURNAL OF NEUROCHEMISTRY, 1993, 61 (06) :2071-2080
[6]   MITOGEN ACTIVATED PROTEIN (MAP) KINASE TRANSFORMS TAU-PROTEIN INTO AN ALZHEIMER-LIKE STATE [J].
DREWES, G ;
LICHTENBERGKRAAG, B ;
DORING, F ;
MANDELKOW, EM ;
BIERNAT, J ;
GORIS, J ;
DOREE, M ;
MANDELKOW, E .
EMBO JOURNAL, 1992, 11 (06) :2131-2138
[7]   TAU-PROTEIN AND THE NEUROFIBRILLARY PATHOLOGY OF ALZHEIMERS-DISEASE [J].
GOEDERT, M .
TRENDS IN NEUROSCIENCES, 1993, 16 (11) :460-465
[8]   THE ABNORMAL PHOSPHORYLATION OF TAU-PROTEIN AT SER-202 IN ALZHEIMER-DISEASE RECAPITULATES PHOSPHORYLATION DURING DEVELOPMENT [J].
GOEDERT, M ;
JAKES, R ;
CROWTHER, RA ;
SIX, J ;
LUBKE, U ;
VANDERMEEREN, M ;
CRAS, P ;
TROJANOWSKI, JQ ;
LEE, VMY .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (11) :5066-5070
[9]   MIGRATION AND AGGREGATION OF EMBRYONIC CHICKEN NEURONS INVITRO - POSSIBLE FUNCTIONAL IMPLICATION OF POLYSIALOGANGLIOSIDES [J].
GREIS, C ;
ROSNER, H .
DEVELOPMENTAL BRAIN RESEARCH, 1990, 57 (02) :223-234
[10]   CHARACTERIZATION OF 2 DISTINCT MONOCLONAL-ANTIBODIES TO PAIRED HELICAL FILAMENTS - FURTHER EVIDENCE FOR FETAL-TYPE PHOSPHORYLATION OF THE TAU IN PAIRED HELICAL FILAMENTS [J].
HASEGAWA, M ;
WATANABE, A ;
TAKIO, K ;
SUZUKI, M ;
ARAI, T ;
TITANI, K ;
IHARA, Y .
JOURNAL OF NEUROCHEMISTRY, 1993, 60 (06) :2068-2077