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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Modulation of the notch signaling by Mash1 and DIx1/2 regulates sequential specification and differentiation of progenitor cell types in the subcortical telencephalon.
Development 129, 5029-5040 (2002)
Notch signaling has a central role in cell fate specification and differentiation. We provide evidence that the Mash1 (bHLH) and Dlx1 and Dlx2 (homeobox) transcription factors have complementary roles in regulating Notch signaling, which in turn mediates the temporal control of subcortical telencephalic neurogenesis in mice. We defined progressively more mature subcortical progenitors (P1, P2 and P3) through their combinatorial expression of MASH1 and DLX2, as well as the expression of proliferative and postmitotic cell markers at E10.5-E11.5. In the absence of Mash1, Notch signaling is greatly reduced and `early' VZ progenitors (P1 and P2) precociously acquire SVZ progenitor (P3) properties. Comparing the molecular phenotypes of the delta-like 1 and Mash1 mutants, suggests that Mash1 regulates early neurogenesis through Notch-and Delta-dependent and -independent mechanisms. While Mash1 is required for early neurogenesis (E10.5), Dlx1 and Dlx2 are required to downregulate Notch signaling during specification and differentiation steps of `late' progenitors (P3). We suggest that alternate cell fate choices in the developing telencephalon are controlled by coordinated functions of bHLH and homeobox transcription factors through their differential affects on Notch signaling.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Mash1 DIx2 Dll1 Telencephalon Notch signaling LGE Striatum Radial glia Neurogenesis Mouse
ISSN (print) / ISBN
0950-1991
e-ISSN
1477-9129
Zeitschrift
Development / Company of Biologists
Quellenangaben
Band: 129,
Heft: 21,
Seiten: 5029-5040
Verlag
Company of Biologists
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Experimental Genetics (IEG)