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Neural Regulation

Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
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Related Experiment Video

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Genetic Manipulation of Cerebellar Granule Neurons In Vitro and In Vivo to Study Neuronal Morphology and Migration
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Cis-regulatory control of corticospinal system development and evolution.

Sungbo Shim1, Kenneth Y Kwan, Mingfeng Li

  • 1Department of Neurobiology and Kavli Institute for Neuroscience, Yale University School of Medicine, New Haven, Connecticut 06510, USA.

Nature
|June 9, 2012
PubMed
Summary

Researchers discovered a gene regulatory element controlling corticospinal neuron development. This element, E4, interacts with SOX transcription factors to ensure proper brain wiring and cortical layer formation in mammals.

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Evolutionary Biology

Background:

  • The mammalian six-layered cerebral neocortex and corticospinal tract are key evolutionary innovations.
  • Genetic mechanisms governing neocortical development and evolution are not fully understood.

Purpose of the Study:

  • To identify genetic elements regulating the development of corticospinal neurons.
  • To elucidate the evolutionary origins of the mammalian neocortex's regulatory networks.

Main Methods:

  • Identification of a conserved non-exonic element (E4) functioning as a cortex-specific enhancer for the Fezf2 gene.
  • Analysis of SOX4, SOX11, and SOX5 interactions with the E4 element.
  • CRISPR-mediated deletion of Sox4 and Sox11 in the cortex to assess effects on Fezf2 expression and neuronal development.
  • Comparative analysis of SOX-binding sites in E4 across tetrapod evolution.

Main Results:

  • E4 acts as a critical enhancer for Fezf2, a gene essential for corticospinal neuron identity.
  • SOX4 and SOX11 activate E4, competing with the repressor SOX5.
  • Deletion of Sox4 and Sox11 disrupts Fezf2 expression, impairs corticospinal neuron specification, and causes reeler-like cortical lamination defects.
  • Evidence suggests the evolution of functional SOX-binding sites in E4 during tetrapod and mammalian evolution.

Conclusions:

  • SOX transcription factors converge on the Fezf2 enhancer E4 to regulate corticospinal neuron development.
  • This regulatory network is crucial for establishing neuronal identity, connectivity, and cortical architecture.
  • The findings provide insights into the genetic basis of mammalian neocortical evolution.