ArticlePloS one2018
Sociability and synapse subtype-specific defects in mice lacking SRPX2, a language-associated gene.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Disruption of cellular iron homeostasis by SRPX2-IRP1 interaction aggravates renal fibrosis in chronic kidney disease.Cell death and differentiation · 2026Article
- Microglia-mediated synaptic pruning in neural circuit remodeling: multidimensional control in homeostasis and neuropathology.BMC medicine · 2026Review
- SOX4 promotes triple-negative breast cancer progression by promoting SRPX2 transcription to regulate AKR1C1.Journal of molecular histology · 2025Article
- A humanized NOVA1 splicing factor alters mouse vocal communications.Nature communications · 2025Article
- Human-Induced Pluripotent Stem Cell (iPSC)-Derived GABAergic Neuron Differentiation in Bipolar Disorder.Cells · 2024Article
- Complement and microglia dependent synapse elimination in brain development.WIREs mechanisms of disease · 2022Review
- Article
- The Ncoa7 locus regulates V-ATPase formation and function, neurodevelopment and behaviour.Cellular and molecular life sciences : CMLS · 2021Article
- The endogenous neuronal complement inhibitor SRPX2 protects against complement-mediated synapse elimination during development.Nature neuroscience · 2020Article
- Genome-Wide Analysis Identifies NURR1-Controlled Network of New Synapse Formation and Cell Cycle Arrest in Human Neural Stem Cells.Molecules and cells · 2020Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The FoxP2 transcription factor and its target genes have been implicated in developmental brain diseases with a prominent language component, such as developmental verbal dyspraxia and specific language impairment. How FoxP2 affects neural circuitry development remains poorly understood. The sushi domain protein SRPX2 is a target of FoxP2, and mutations in SRPX2 are associated with language defects in humans. We have previously shown that SRPX2 is a synaptogenic protein that increases excitatory synapse density. Here we provide the first characterization of mice lacking the SRPX2 gene, and show that these mice exhibit defects in both neural circuitry and communication and social behaviors. Specifically, we show that mice lacking SRPX2 show a specific reduction in excitatory VGlut2 synapses in the cerebral cortex, while VGlut1 and inhibitory synapses were largely unaffected. SRPX2 KO mice also exhibit an abnormal ultrasonic vocalization ontogenetic profile in neonatal pups, and reduced preference for social novelty. These data demonstrate a functional role for SRPX2 during brain development, and further implicate FoxP2 and its targets in regulating the development of vocalization and social circuits.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.