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

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 <i>FOXP2</i> are associated with severe developmental speech disturbances, and molecular studies indicate that impairment of <i>Foxp2</i> 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, <i>Foxp2</i> 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 <i>Foxp2</i> 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.