Mammalian Par3 regulates progenitor cell asymmetric division via notch signaling in the developing neocortex. Bultje, R. S, Castaneda-Castellanos, D. R, Jan, L. Y., Jan, Y., Kriegstein, A. R, & Shi, S. Neuron, 63(2):189–202, July, 2009. abstract bibtex 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.
@ARTICLE{Bultje2009-tx,
title = "Mammalian Par3 regulates progenitor cell asymmetric division via
notch signaling in the developing neocortex",
author = "Bultje, Ronald S and Castaneda-Castellanos, David R and Jan, Lily
Yeh and Jan, Yuh-Nung and Kriegstein, Arnold R and Shi, Song-Hai",
abstract = "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.",
journal = "Neuron",
volume = 63,
number = 2,
pages = "189--202",
month = jul,
year = 2009,
language = "en"
}
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