Mammalian Par3 Regulates Progenitor Cell Asymmetric Division via Notch Signaling in the Developing Neocortex

被引:260
作者
Bultje, Ronald S. [1 ,2 ]
Castaneda-Castellanos, David R. [3 ,4 ]
Jan, Lily Yen [5 ,6 ,7 ]
Jan, Yuh-Nung [5 ,6 ,7 ]
Kriegstein, Arnold R. [4 ]
Shi, Song-Hai [1 ]
机构
[1] Mem Sloan Kettering Canc Ctr, Dev Biol Program, New York, NY 10065 USA
[2] Cornell Univ, Weill Med Coll, Dept Pharmacol, New York, NY 10065 USA
[3] Columbia Univ, Dept Physiol & Cellular Biophys, New York, NY 10032 USA
[4] Univ Calif San Francisco, Sch Med, Dept Neurol, San Francisco, CA 94143 USA
[5] Univ Calif San Francisco, Howard Hughes Med Inst, Dept Physiol, San Francisco, CA 94143 USA
[6] Univ Calif San Francisco, Howard Hughes Med Inst, Dept Biochem, San Francisco, CA 94143 USA
[7] Univ Calif San Francisco, Howard Hughes Med Inst, Dept Biophys, San Francisco, CA 94143 USA
关键词
RADIAL GLIAL-CELLS; CENTRAL-NERVOUS-SYSTEM; NEURAL STEM-CELLS; CORTICAL NEUROGENESIS; CEREBRAL-CORTEX; NEUROEPITHELIAL CELLS; MOUSE NUMB; INTERMEDIATE PROGENITORS; NEURONS ARISE; POLARITY;
D O I
10.1016/j.neuron.2009.07.004
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Asymmetric cell division of radial glial progenitors produces neurons while allowing self-renewal; however, little is known about the mechanism that generates asymmetry in daughter cell fate specification. Here, we found that mammalian partition defective protein 3 (mPar3), a key cell polarity determinant, exhibits dynamic distribution in radial glial progenitors. While it is enriched at the lateral membrane domain in the ventricular endfeet during interphase, mPar3 becomes dispersed and shows asymmetric localization as cell cycle progresses. Either removal or ectopic expression of mPar3 prevents radial glial progenitors from dividing asymmetrically yet generates different outcomes in daughter cell fate specification. Furthermore, the expression level of mPar3 affects Notch signaling, and manipulations of Notch signaling or Numb expression suppress mPar3 regulation of radial glial cell division and daughter cell fate specification. These results reveal a critical molecular pathway underlying asymmetric cell division of radial glial progenitors in the mammalian neocortex.
引用
收藏
页码:189 / 202
页数:14
相关论文
共 67 条
[11]  
2-4
[12]   Neurons from radial glia: the consequences of asymmetric inheritance [J].
Fishell, G ;
Kriegstein, AR .
CURRENT OPINION IN NEUROBIOLOGY, 2003, 13 (01) :34-41
[13]   The role of Notch in promoting glial and neural stem cell fates [J].
Gaiano, N ;
Fishell, G .
ANNUAL REVIEW OF NEUROSCIENCE, 2002, 25 :471-490
[14]   Radial glial identity is promoted by Notch1 signaling in the murine forebrain [J].
Gaiano, N ;
Nye, JS ;
Fishell, G .
NEURON, 2000, 26 (02) :395-404
[15]   Neurons arise in the basal neuroepithelium of the early mammalian telencephalon: A major site of neurogenesis [J].
Haubensak, W ;
Attardo, A ;
Denk, W ;
Huttner, WB .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (09) :3196-3201
[16]   Mitotic spindle rotation and mode of cell division in the developing telencephalon [J].
Haydar, TF ;
Ang, E ;
Rakic, P .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (05) :2890-2895
[17]   An atypical PKC directly associates and colocalizes at the epithelial tight junction with ASIP, a mammalian homologue of Caenorhabditis elegans polarity protein PAR-3 [J].
Izumi, Y ;
Hirose, T ;
Tamai, Y ;
Hirai, S ;
Nagashima, Y ;
Fujimoto, T ;
Tabuse, Y ;
Kemphues, KJ ;
Ohno, S .
JOURNAL OF CELL BIOLOGY, 1998, 143 (01) :95-106
[18]   Asymmetric cell division in the Drosophila nervous system [J].
Jan, YN ;
Jan, LY .
NATURE REVIEWS NEUROSCIENCE, 2001, 2 (11) :772-779
[19]   The cell-polarity protein Par6 links Par3 and atypical protein kinase C to Cdc42 [J].
Joberty, G ;
Petersen, C ;
Gao, L ;
Macara, IG .
NATURE CELL BIOLOGY, 2000, 2 (08) :531-539
[20]  
Johansson AS, 2000, J CELL SCI, V113, P3267