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Mash1 regulates neurogenesis in the ventral telencephalon

Casarosa, Simona, Fode, Carol, Guillemot, François·1999·Development
DOI 10.1242/dev.126.3.525
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Abstract

Previous studies have shown that mice mutant for the gene Mash1 display severe neuronal losses in the olfactory epithelium and ganglia of the autonomic nervous system, demonstrating a role for Mash1 in development of neuronal lineages in the peripheral nervous system. Here, we have begun to analyse Mash1 function in the central nervous system, focusing our studies on the ventral telencephalon where it is expressed at high levels during neurogenesis. Mash1 mutant mice present a severe loss of progenitors, particularly of neuronal precursors in the subventricular zone of the medial ganglionic eminence. Discrete neuronal populations of the basal ganglia and cerebral cortex are subsequently missing. An analysis of candidate effectors of Mash1 function revealed that the Notch ligands Dll1 and Dll3, and the target of Notch signaling Hes5, fail to be expressed in Mash1 mutant ventral telencephalon. In the lateral ganglionic eminence, loss of Notch signaling activity correlates with premature expression of a number of subventricular zone markers by ventricular zone cells. Therefore, Mash1 is an important regulator of neurogenesis in the ventral telencephalon, where it is required both to specify neuronal precursors and to control the timing of their production.

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Metadata

Authors
Casarosa, S., Fode, C., & Guillemot, F.
Venue
Development
Publisher
The Company of Biologists
Published
1999-02-01
Volume
126
Issue
3
Pages
525-534
ISSN
  • 0950-1991 (ISSN-L)
  • 1477-9129
DOI
10.1242/dev.126.3.525
OpenAlex
W2138921976
Cited by
639
References
0
FWCI
6.78
Type
journal article
Language
en
Open access
closed

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