| Autor: |
Molyneaux BJ; MGH-HMS Center for Nervous System Repair, Department of Neurosurgery, Program in Neuroscience and Harvard Stem Cell Institute, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts 02114, USA., Arlotta P, Hirata T, Hibi M, Macklis JD |
| Jazyk: |
angličtina |
| Zdroj: |
Neuron [Neuron] 2005 Sep 15; Vol. 47 (6), pp. 817-31. |
| DOI: |
10.1016/j.neuron.2005.08.030 |
| Abstrakt: |
The molecular mechanisms controlling the differentiation of neural progenitors into distinct subtypes of neurons during neocortical development are unknown. Here, we report that Fezl is required for the specification of corticospinal motor neurons and other subcerebral projection neurons, which are absent from Fezl null mutant neocortex. There is neither an increase in cell death in Fezl(-/-) cortex nor abnormalities in migration, indicating that the absence of subcerebral projection neurons is due to a failure in fate specification. In striking contrast, other neuronal populations in the same and other cortical layers are born normally. Overexpression of Fezl results in excess production of subcerebral projection neurons and arrested migration of these neurons in the germinal zone. These data indicate that Fezl plays a central role in the specification of corticospinal motor neurons and other subcerebral projection neurons, controlling early decisions regarding lineage-specific differentiation from neural progenitors. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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