Increased neuronal production, enlarged forebrains and cytoarchitectural distortions in β-catenin overexpressing transgenic mice

被引:205
作者
Chenn, A
Walsh, CA
机构
[1] Northwestern Univ, Feinberg Sch Med, Dept Pathol, Chicago, IL 60611 USA
[2] Harvard Univ, Beth Israel Deaconess Med Ctr, Howard Hughes Med Inst, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA
关键词
D O I
10.1093/cercor/13.6.599
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
beta-Catenin can function in the decision of neural precursors to proliferate or differentiate during mammalian neuronal development and may regulate cerebral cortical size by controlling the generation of neural precursor cells. Mice expressing high levels of a stabilized beta-catenin transgene in neural precursors develop enlarged brains with expanded precursor populations, increased cerebral cortical surface area, and folds resembling sulci and gyri of higher mammals present at birth. Here we report the effects in adult mice expressing lower levels of the same stabilized beta-catenin transgene in neural precursors. Adult transgenic animals develop enlarged forebrains with thin cerebral cortices with increased surface area, expanded subventricular zones with subcortical aggregations of neurons and enlarged, distorted hippocampi. The brains from transgenic mice also show apparent arrest of neuronal migration and dramatic disorganization of the layering of the cerebral cortex. These findings suggest that beta-catenin can cause expansion of the precursor pool resulting in increased neuronal production and greater brain size and suggest a crucial role for beta-catenin in neuronal migration and cortical lamination.
引用
收藏
页码:599 / 606
页数:8
相关论文
共 32 条
[1]   Neurogenesis in adult subventricular zone [J].
Alvarez-Buylla, A ;
García-Verdugo, JM .
JOURNAL OF NEUROSCIENCE, 2002, 22 (03) :629-634
[2]  
Anderson SA, 2001, DEVELOPMENT, V128, P353
[3]   NH2-terminal deletion of beta-catenin results in stable colocalization of mutant beta-catenin with adenomatous polyposis coli protein and altered MDCK cell adhesion [J].
Barth, AIM ;
Pollack, AL ;
Altschuler, Y ;
Mostov, KE ;
Nelson, WJ .
JOURNAL OF CELL BIOLOGY, 1997, 136 (03) :693-706
[4]   Mosaic evolution of brain structure in mammals [J].
Barton, RA ;
Harvey, PH .
NATURE, 2000, 405 (6790) :1055-1058
[5]   Differential distribution of the glutamate transporters GLT-1 and GLAST in tanycytes of the third ventricle [J].
Berger, UV ;
Hediger, MA .
JOURNAL OF COMPARATIVE NEUROLOGY, 2001, 433 (01) :101-114
[6]  
Brault V, 2001, DEVELOPMENT, V128, P1253
[7]   T-BRAIN-1 - A HOMOLOG OF BRACHYURY WHOSE EXPRESSION DEFINES MOLECULARLY DISTINCT DOMAINS WITHIN THE CEREBRAL-CORTEX [J].
BULFONE, A ;
SMIGA, SM ;
SHIMAMURA, K ;
PETERSON, A ;
PUELLES, L ;
RUBENSTEIN, JLR .
NEURON, 1995, 15 (01) :63-78
[8]   NUMBERS, TIME AND NEOCORTICAL NEURONOGENESIS - A GENERAL DEVELOPMENTAL AND EVOLUTIONARY MODEL [J].
CAVINESS, VS ;
TAKAHASHI, T ;
NOWAKOWSKI, RS .
TRENDS IN NEUROSCIENCES, 1995, 18 (09) :379-383
[9]   Regulation of cerebral cortical size by control of cell cycle exit in neural precursors [J].
Chenn, A ;
Walsh, CA .
SCIENCE, 2002, 297 (5580) :365-369
[10]  
Cho EA, 1998, MECH DEVELOP, V77, P9