The Specification of Cortical Subcerebral Projection Neurons Depends on the Direct Repression of TBR1 by CTIP1/BCL11a

The acquisition of distinct neuronal fates is fundamental for the function of the cerebral cortex. We find that the development of subcerebral projections from layer 5 neurons in the mouse neocortex depends on the high levels of expression of the transcription factor CTIP1; CTIP1 is coexpressed with...

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Bibliographic Details
Published in:The Journal of neuroscience 2015-05, Vol.35 (19), p.7552-7564
Main Authors: Cánovas, José, Berndt, F Andrés, Sepúlveda, Hugo, Aguilar, Rodrigo, Veloso, Felipe A, Montecino, Martín, Oliva, Carlos, Maass, Juan C, Sierralta, Jimena, Kukuljan, Manuel
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
Carrier Proteins - genetics
Carrier Proteins - metabolism
Cells, Cultured
Cerebral Cortex - cytology
Cerebral Cortex - embryology
Cerebral Cortex - growth & development
DNA-Binding Proteins - metabolism
Embryo, Mammalian
Female
Gene Expression Regulation, Developmental - genetics
Histones - metabolism
Humans
In Vitro Techniques
Ki-67 Antigen - metabolism
Male
Mice
Mice, Transgenic
Microtubule-Associated Proteins - metabolism
Neural Pathways - physiology
Neurons - physiology
Neuropeptides - metabolism
Nuclear Proteins - genetics
Nuclear Proteins - metabolism
T-Box Domain Proteins - metabolism
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Summary:The acquisition of distinct neuronal fates is fundamental for the function of the cerebral cortex. We find that the development of subcerebral projections from layer 5 neurons in the mouse neocortex depends on the high levels of expression of the transcription factor CTIP1; CTIP1 is coexpressed with CTIP2 in neurons that project to subcerebral targets and with SATB2 in those that project to the contralateral cortex. CTIP1 directly represses Tbr1 in layer 5, which appears as a critical step for the acquisition of the subcerebral fate. In contrast, lower levels of CTIP1 in layer 6 are required for TBR1 expression, which directs the corticothalamic fate. CTIP1 does not appear to play a critical role in the acquisition of the callosal projection fate in layer 5. These findings unravel a key step in the acquisition of cell fate for closely related corticofugal neurons and indicate that differential dosages of transcriptions factors are critical to specify different neuronal identities.
ISSN:0270-6474
1529-2401
DOI:10.1523/JNEUROSCI.0169-15.2015