Control of outer radial glial stem cell mitosis in the human brain. Ostrem, B. E L, Lui, J. H, Gertz, C. C, & Kriegstein, A. R Cell Rep, 8(3):656–664, July, 2014. abstract bibtex Evolutionary expansion of the human neocortex is partially attributed to a relative abundance of neural stem cells in the fetal brain called outer radial glia (oRG). oRG cells display a characteristic division mode, mitotic somal translocation (MST), in which the soma rapidly translocates toward the cortical plate immediately prior to cytokinesis. MST may be essential for progenitor zone expansion, but the mechanism of MST is unknown, hindering exploration of its function in development and disease. Here, we show that MST requires activation of the Rho effector ROCK and nonmuscle myosin II, but not intact microtubules, centrosomal translocation into the leading process, or calcium influx. MST is independent of mitosis and distinct from interkinetic nuclear migration and saltatory migration. Our findings suggest that disrupted MST may underlie neurodevelopmental diseases affecting the Rho-ROCK-myosin pathway and provide a foundation for future exploration of the role of MST in neocortical development, evolution, and disease.
@ARTICLE{Ostrem2014-ds,
title = "Control of outer radial glial stem cell mitosis in the human
brain",
author = "Ostrem, Bridget E L and Lui, Jan H and Gertz, Caitlyn C and
Kriegstein, Arnold R",
abstract = "Evolutionary expansion of the human neocortex is partially
attributed to a relative abundance of neural stem cells in the
fetal brain called outer radial glia (oRG). oRG cells display a
characteristic division mode, mitotic somal translocation (MST),
in which the soma rapidly translocates toward the cortical plate
immediately prior to cytokinesis. MST may be essential for
progenitor zone expansion, but the mechanism of MST is unknown,
hindering exploration of its function in development and disease.
Here, we show that MST requires activation of the Rho effector
ROCK and nonmuscle myosin II, but not intact microtubules,
centrosomal translocation into the leading process, or calcium
influx. MST is independent of mitosis and distinct from
interkinetic nuclear migration and saltatory migration. Our
findings suggest that disrupted MST may underlie
neurodevelopmental diseases affecting the Rho-ROCK-myosin pathway
and provide a foundation for future exploration of the role of
MST in neocortical development, evolution, and disease.",
journal = "Cell Rep",
volume = 8,
number = 3,
pages = "656--664",
month = jul,
year = 2014,
language = "en"
}
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