FOXP2 exhibits neuron class specific expression, but is not required for multiple aspects of cortical histogenesis

  1. Ryan J Kast  Is a corresponding author
  2. Alexandra L Lanjewar
  3. Colton D Smith
  4. Pat Levitt  Is a corresponding author
  1. University of Southern California, United States
  2. Children's Hospital Los Angeles, United States

Abstract

The expression patterns of the transcription factor FOXP2 in the developing mammalian forebrain have been described, and some studies have tested the role of this protein in the development and function of specific forebrain circuits by diverse methods and in multiple species. Clinically, mutations in FOXP2 are associated with severe developmental speech disturbances, and molecular studies indicate that impairment of Foxp2 may lead to dysregulation of genes involved in forebrain histogenesis. Here, anatomical and molecular phenotypes of the cortical neuron populations that express FOXP2 were characterized in mice. Additionally, Foxp2 was removed from the developing mouse cortex at different prenatal ages using two Cre-recombinase driver lines. Detailed molecular and circuit analyses were undertaken to identify potential disruptions of development. Surprisingly, the results demonstrate that Foxp2 function is not required for many functions that it has been proposed to regulate, and therefore plays a more limited role in cortical development than previously thought.

Data availability

All numbers relating to quantitative experiments have been uploaded to Dryad. https://dx.doi.org/10.5061/dryad.6hd7bf7

The following data sets were generated

Article and author information

Author details

  1. Ryan J Kast

    Keck School of Medicine, University of Southern California, Los Angeles, United States
    For correspondence
    rkast@mit.edu
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-3580-8811
  2. Alexandra L Lanjewar

    Keck School of Medicine, University of Southern California, Los Angeles, United States
    Competing interests
    The authors declare that no competing interests exist.
  3. Colton D Smith

    Keck School of Medicine, University of Southern California, Los Angeles, United States
    Competing interests
    The authors declare that no competing interests exist.
  4. Pat Levitt

    The Saban Research Institute, Children's Hospital Los Angeles, Los Angeles, United States
    For correspondence
    plevitt@med.usc.edu
    Competing interests
    The authors declare that no competing interests exist.

Funding

National Institute of Mental Health (MH067842)

  • Ryan J Kast
  • Alexandra L Lanjewar
  • Colton D Smith
  • Pat Levitt

Children's Hospital Los Angeles

  • Ryan J Kast

Simms/Mann Institute and Foundation

  • Pat Levitt

National Institutes of Health (T32GM113859)

  • Alexandra L Lanjewar

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

  1. Constance L Cepko, Harvard Medical School, United States

Ethics

Animal experimentation: All animal procedures used in this study were in strict accordance with the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. The protocol was approved by the Institutional Animal Care and Use Committee at Children's Hospital Los Angeles (Protocol #374-15).

Version history

  1. Received: September 14, 2018
  2. Accepted: May 14, 2019
  3. Accepted Manuscript published: May 17, 2019 (version 1)
  4. Version of Record published: June 12, 2019 (version 2)

Copyright

© 2019, Kast et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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  1. Ryan J Kast
  2. Alexandra L Lanjewar
  3. Colton D Smith
  4. Pat Levitt
(2019)
FOXP2 exhibits neuron class specific expression, but is not required for multiple aspects of cortical histogenesis
eLife 8:e42012.
https://doi.org/10.7554/eLife.42012

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https://doi.org/10.7554/eLife.42012