Abstract:

Forkhead box protein P1 (FOXP1) is a transcription factor belonging to the forkhead box (FOX) proteins, a family of transcriptional regulators sharing a highly conserved forkhead DNA-binding domain (Bacon and Rappold, 2012). Previous reports have proposed a role for FOXP1 in functionally regulating the central nervous system (CNS), while mutations in FOXP1 have been implicated in cognitive abnormalities (Bacon and Rappold, 2012). FOXP1 has been shown to promote differentiation of medium spiny neurons and to induce neuronal migration during embryonic neuronal development in the mouse cortex (Li et al., 2015; Precious et al., 2016). Mutations in FOXP1 have been linked to various neurodevelopmental diseases, including autism, intellectual disabilities and speech defects (Hamdan et al., 2010; Horn et al., 2010). Furthermore, Bacon and colleagues demonstrated that Cre-mediated Foxp1 deletion in Nestin-positive cells induces autism-like behavior in mice, and defects in morphology of the striatum upon postnatal development (Bacon et al., 2015). In line with these findings, heterozygous Foxp1+/– mice have been reported to show deficits in vocal communication as well as a deregulation of autism-associated genes in the hippocampus and striatum (Araujo et al.,2015). Taken together, this body of evidence indicates an important role of FOXP1 in regulating CNS development, however the molecular mechanisms underlying neuronal FOXP1 function have remained unclear.