RNA-seq Re-analysis of FOXP1 KO Identifies Synaptic Dysfunction in a Model of Communication Disorders

Publication Date

2026

College

College of Sciences & Mathematics

Department

Psychological Sciences and Neurosciences, Department of

Student Level

Undergraduate

Faculty Mentor

Jinhee Park

Presentation Type

Poster

Summary

Communication disorders are characterized by difficulties in speech and language use, often leading to social and cognitive challenges. These disorders are associated with underlying biological changes in the developing brain, making it important to understand their molecular mechanisms to identify potential therapeutic targets.

In this study, we re-analyzed publicly available RNA-seq data from a FOXP1 knockout (KO) model to investigate gene expression changes associated with communication disorders in the cortex. FOXP1 is a transcription factor critical for brain development and has been strongly linked to speech and language disorders. Differential expression analysis was performed using edgeR to compare KO and control conditions.

Using a false discovery rate (FDR) cutoff of 0.05, a total of 1405 differentially expressed genes (DEGs) were identified at P0 and 622 DEGs at P7, indicating stronger transcriptional disruption at earlier developmental stages. Consistently, Venn diagram analysis showed limited overlap between the two time points, with only 169 shared DEGs, while 1236 genes were unique to P0 and 453 genes were unique to P7, suggesting stage-specific transcriptional regulation following FOXP1 loss.

To understand the biological pathways associated with these gene expression changes at P7, pathway (Gene Ontology) enrichment analysis was performed. Upregulated genes were primarily associated with response to estradiol and developmental processes, while downregulated genes were strongly enriched in pathways related to synaptic transmission, including neurotransmitter transport, synaptic plasticity, and axonogenesis, particularly within glutamatergic signaling.

These findings suggest that FOXP1 loss disrupts synaptic transmission pathways, which may underlie the communication deficits observed in this model.

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