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Selective induction of neocortical GABAergic neurons by the PDK1-Akt pathway through activation of Mash1.

Abstract：

:Extracellular stimuli regulate neuronal differentiation and subtype specification during brain development, although the intracellular signaling pathways that mediate these processes remain largely unclear. We now show that the PDK1-Akt pathway regulates differentiation of telencephalic neural precursor cells (NPCs). Active Akt promotes differentiation of NPC into gamma-aminobutyric acid-containing (GABAergic) but not glutamatergic neurons. Disruption of the Pdk1 gene or expression of dominant-negative forms of Akt suppresses insulin-like growth factor (IGF)-1 enhancement of NPC differentiation into neurons in vitro and production of neocortical GABAergic neurons in vivo. Furthermore, active Akt increased the protein levels and transactivation activity of Mash1, a proneural basic helix-loop-helix protein required for the generation of neocortical GABAergic neurons, and Mash1 was required for Akt-induced neuronal differentiation. These results have unveiled an unexpected role of the PDK1-Akt pathway: a key mediator of extracellular signals regulating the production of neocortical GABAergic neurons.

journal_name

Proc Natl Acad Sci U S A

journal_title

Proceedings of the National Academy of Sciences of the United States of America

authors

Oishi K,Watatani K,Itoh Y,Okano H,Guillemot F,Nakajima K,Gotoh Y

doi

10.1073/pnas.0808400106

subject

Has Abstract

pub_date

2009-08-04 00:00:00

pages

13064-9

issue

31

eissn

0027-8424

issn

1091-6490

pii

0808400106

journal_volume

106

pub_type

杂志文章

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