Mice carrying a humanized Foxp2 knock-in allele show region-specific shifts of striatal Foxp2 expression levels
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چکیده
منابع مشابه
Generation of mice with a conditional Foxp2 null allele
Disruptions of the human FOXP2 gene cause problems with articulation of complex speech sounds, accompanied by impairment in many aspects of language ability. The FOXP2/Foxp2 transcription factor is highly similar in humans and mice, and shows a complex conserved expression pattern, with high levels in neuronal subpopulations of the cortex, striatum, thalamus, and cerebellum. In the present stud...
متن کاملFoxp2
The forkhead box P2 gene, designated FOXP2, is the first gene implicated in a speech and language disorder. Since its discovery, many studies have been carried out in an attempt to explain the mechanism by which it influences these characteristically human traits. This review presents the story of the discovery of the FOXP2 gene, including early studies of the phenotypic implications of a disru...
متن کاملA Humanized Version of Foxp2 Affects Cortico-Basal Ganglia Circuits in Mice
It has been proposed that two amino acid substitutions in the transcription factor FOXP2 have been positively selected during human evolution due to effects on aspects of speech and language. Here, we introduce these substitutions into the endogenous Foxp2 gene of mice. Although these mice are generally healthy, they have qualitatively different ultrasonic vocalizations, decreased exploratory b...
متن کاملFOXP2 targets show evidence of positive selection in European populations.
Forkhead box P2 (FOXP2) is a highly conserved transcription factor that has been implicated in human speech and language disorders and plays important roles in the plasticity of the developing brain. The pattern of nucleotide polymorphisms in FOXP2 in modern populations suggests that it has been the target of positive (Darwinian) selection during recent human evolution. In our study, we searche...
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ژورنال
عنوان ژورنال: Cortex
سال: 2019
ISSN: 0010-9452
DOI: 10.1016/j.cortex.2019.01.008