ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
The Specification of Cortical Subcerebral Projection Neurons Depends on the Direct Repression of TBR1 by CTIP1/BCL11a.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 65 citations in OpenAlex.
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- Tbr1 Misexpression Alters Neuronal Development in the Cerebral Cortex.Molecular neurobiology · 2022Article
- Transcription factors Bcl11a and Bcl11b are required for the production and differentiation of cortical projection neurons.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Rpsa Signaling Regulates Cortical Neuronal Morphogenesis via Its Ligand, PEDF, and Plasma Membrane Interaction Partner, Itga6.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
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- Developmental and Behavioral Phenotypes in a Mouse Model of DDX3X Syndrome.Biological psychiatry · 2021Article
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- Human Pluripotent Stem Cell-Derived Neurons Are Functionally Mature In Vitro and Integrate into the Mouse Striatum Following Transplantation.Molecular neurobiology · 2020Article
- Generating homogenous cortical preplate and deep-layer neurons using a combination of 2D and 3D differentiation cultures.Scientific reports · 2020Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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