| Experiment Id | GSE228825 | Name | Foxp striatal compensation (RNA-Seq) |
| Experiment Type | RNA-Seq | Study Type | WT vs. Mutant |
| Source | GEO | Curation Date | 2024-08-27 |
| description | Spiny projection neurons (SPNs) of the striatum are critical in integrating neurochemical information to coordinate motor and reward-based behavior. Mutations in the regulatory transcription factors expressed in SPNs can result in neurodevelopmental disorders (NDDs). Paralogous transcription factors Foxp1andFoxp2, which are both expressed in the dopamine receptor 1 (D1) expressing SPNs, are known to have variants implicated in NDDs. Utilizing mice with a D1-SPN specific loss of Foxp1,Foxp2, or both and a combination of behavior, electrophysiology, and single-nuclei RNA (snRNA-seq) and single-nuclei Assay for Transposase-Accessible Chromatin sequencing (snATAC-seq), we find that loss of both genes results in impaired motor and social behavior as well as increased firing of the D1-SPNs. Differential gene expression analysis of snRNA-seq data implicates genes involved in autism risk, altered electrophysiological properties, and neuronal development and function. These data indicate complementary roles between Foxp1 and Foxp2 in the D1-SPNs. The transcription factors Foxp1 and Foxp2 are both expressed in the D1-SPNs of the striatum. We used single nuclei RNA sequencing (snRNA-Seq) in both juvenile (P9) and adult (P56) mouse striatum to test the effects of loss of one or both of these genes from the D1-SPNs. |
