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Related Experiment Video

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Mob2 Insufficiency Disrupts Neuronal Migration in the Developing Cortex.

Adam C O'Neill1,2, Christina Kyrousi3, Melanie Einsiedler2

  • 1Department of Women's and Children's Health, University of Otago, Dunedin, New Zealand.

Frontiers in Cellular Neuroscience
|March 30, 2018
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Summary
This summary is machine-generated.

Genetic variants in MOB2 cause neuronal mispositioning disorders like periventricular nodular heterotopia (PH). This study confirms MOB2

Keywords:
Hippo pathwayMob2cortical developmentexome sequencingperiventricular heterotopia

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Area of Science:

  • Neuroscience and Genetics
  • Developmental Biology

Background:

  • Neuronal mispositioning disorders during brain development have unknown genetic causes.
  • Periventricular nodular heterotopia (PH) is a disorder characterized by misplaced neurons.

Purpose of the Study:

  • To investigate the genetic basis of neuronal mispositioning disorders.
  • To identify novel genes associated with periventricular nodular heterotopia (PH).

Main Methods:

  • Genetic and cellular analysis of biallelic variants in the Hippo signaling factor MOB2.
  • Loss-of-function studies using knockdown of Mob2 in developing mouse cortex.
  • Assessment of cilia positioning, number, and Filamin A phosphorylation.

Main Results:

  • Biallelic MOB2 variants identified in a PH patient were confirmed as loss-of-function.
  • Mob2 knockdown in mice impaired neuronal positioning and cilia defects.
  • Reduced Mob2 expression affected Filamin A phosphorylation, a protein implicated in PH.

Conclusions:

  • MOB2 plays a critical role in neuronal positioning during cortical development.
  • MOB2 variants represent a new potential genetic cause for periventricular nodular heterotopia (PH).