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Coordination of Neuron Production in Mouse and Human Cerebral Cortex by the Homolog of Drosophila Mastermind Protein.

Brain Behav Evol. 2019;93(2-3):152-165. Epub 2019 Aug 15
Albert E Ayoub 1 , Martin H Dominguez 2 , Jaime Benoit 3 , Juan Alberto Ortega 4 , Nevena Radonjic 5 , Nada Zecevic 6 , Pasko Rakic 7
Albert E Ayoub 1 , Martin H Dominguez 2 , Jaime Benoit 3 , Juan Alberto Ortega 4 , Nevena Radonjic 5 , Nada Zecevic 6 , Pasko Rakic 7
+ et al

[No authors listed]

Author information
  • 1 Department of Neuroscience and Kavli Institute for Neuroscience, Yale University, New Haven, Connecticut, USA.
  • 2 Medical Training Program, Yale University, New Haven, Connecticut, USA.
  • 3 Department of Psychology, Yale University, New Haven, Connecticut, USA.
  • 4 The Ken & Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
  • 5 Department of Psychiatry, SUNY Upstate Medical University, Syracuse, New York, USA.
  • 6 UCONN Health Science Center, University of Connecticut, Farmington, Connecticut, USA.
  • 7 Department of Neuroscience and Kavli Institute for Neuroscience, Yale University, New Haven, Connecticut, USA, pasko.rakic@yale.edu.

摘要

The coordination of progenitor self-renewal, neuronal production, and migration is essential to the normal development and evolution of the cerebral cortex. Numerous studies have shown that the Notch, Wnt/beta-catenin, and Neurogenin pathways contribute separately to progenitor expansion, neurogenesis, and neuronal migration, but it is unknown how these signals are coordinated. In vitro studies suggested that the mastermind-like 1 (MAML1) gene, homologue of the Drosophila mastermind, plays a role in coordinating the aforementioned signaling pathways, yet its role during cortical development remains largely unknown. Here we show that ectopic expression of dominant-negative MAML (dnMAML) causes exuberant neuronal production in the mouse cortex without disrupting neuronal migration. Comparing the transcriptional consequences of dnMAML and Neurog2 ectopic expression revealed a complex genetic network controlling the balance of progenitor expansion versus neuronal production. Manipulation of MAML and Neurog2 in cultured human cerebral stem cells exposed interactions with the same set of signaling pathways. Thus, our data suggest that evolutionary changes that affect the timing, tempo, and density of successive neuronal layers of the small lissencephalic rodent and large convoluted primate cerebral cortex depend on similar molecular mechanisms that act from the earliest developmental stages.

KEYWORDS: Cortical evolution, In utero electroporation, Mastermind-like 1, Neurogenin 2, Neuronal migration, Notch

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