Potential role of SLC6A3 in neurodevelopmental impairments associated with corpus callosum abnormalities: insights from CNV analysis and clinical phenotyping

Abstract Objective This study aimed to investigate the role of pathogenic copy number variations (CNVs) in neurodevelopmental impairments among children with corpus callosum abnormalities (CCAs). We focused primarily on SLC6A3 associated mechanisms and aimed to delineate genotype-phenotype correlati...

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Main Authors: Shan-yu Liu, Wei Huang, Hui-lin Ou, Li Wang, Dan-dan Wang, Wei-he Tan, Qin She
Format: Article
Language:English
Published: BMC 2025-08-01
Series:Molecular Cytogenetics
Online Access:https://doi.org/10.1186/s13039-025-00725-4
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author Shan-yu Liu
Wei Huang
Hui-lin Ou
Li Wang
Dan-dan Wang
Wei-he Tan
Qin She
author_facet Shan-yu Liu
Wei Huang
Hui-lin Ou
Li Wang
Dan-dan Wang
Wei-he Tan
Qin She
author_sort Shan-yu Liu
collection DOAJ
description Abstract Objective This study aimed to investigate the role of pathogenic copy number variations (CNVs) in neurodevelopmental impairments among children with corpus callosum abnormalities (CCAs). We focused primarily on SLC6A3 associated mechanisms and aimed to delineate genotype-phenotype correlations in our cases. Methods From January 2021 to July 2023, 13 children with MRI-confirmed CCAs underwent chromosomal microarray analysis (CMA) for CNV detection. We performed bioinformatic analyses (Gene Ontology, STRING network) to identify neurodevelopmental genes within pathogenic CNVs, and clinical follow up assessed neurobehavioral outcomes. Results We identified pathogenic CNVs in 3/13 cases (23.08%). Specifically, Case 8 harbored a 43.05-Mb duplication (5p15.33p12) encompassing SLC6A3, a dopamine transporter gene linked to synaptic signaling. Interaction network analysis suggested that SLC6A3 was the most interconnected gene, providing evidence of its role in CCAs. Clinically, 84.6% of cases (11/13) exhibited psychomotor delay, while 15.4% of cases (2/13) developed seizure. Notably, we observed hearing impairment and psychomotor developmental delay in Case 8 with a SLC6A3 duplication, further suggesting dopaminergic dysregulation in callosal connectivity. Conclusion Our study suggests that SLC6A3 may represent a potential contributor to neurodevelopmental impairments in CCAs. Further, CMA-based CNV screening is critical for early intervention in high-risk children. These findings bridge genetic etiology with clinical phenotypes and offer insights into future targeted therapeutic strategies.
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spelling doaj-art-e51c7454f5a5405e8e1ae01db107d0322025-08-24T11:52:15ZengBMCMolecular Cytogenetics1755-81662025-08-011811810.1186/s13039-025-00725-4Potential role of SLC6A3 in neurodevelopmental impairments associated with corpus callosum abnormalities: insights from CNV analysis and clinical phenotypingShan-yu Liu0Wei Huang1Hui-lin Ou2Li Wang3Dan-dan Wang4Wei-he Tan5Qin She6Prenatal Diagnostic Center, the Affiliated Qingyuan Hospital, Guangzhou Medical University (Qingyuan People’s Hospital)Prenatal Diagnostic Center, the Affiliated Qingyuan Hospital, Guangzhou Medical University (Qingyuan People’s Hospital)Prenatal Diagnostic Center, the Affiliated Qingyuan Hospital, Guangzhou Medical University (Qingyuan People’s Hospital)Prenatal Diagnostic Center, the Affiliated Qingyuan Hospital, Guangzhou Medical University (Qingyuan People’s Hospital)Prenatal Diagnostic Center, the Affiliated Qingyuan Hospital, Guangzhou Medical University (Qingyuan People’s Hospital)Prenatal Diagnostic Center, the Affiliated Qingyuan Hospital, Guangzhou Medical University (Qingyuan People’s Hospital)Prenatal Diagnostic Center, the Affiliated Qingyuan Hospital, Guangzhou Medical University (Qingyuan People’s Hospital)Abstract Objective This study aimed to investigate the role of pathogenic copy number variations (CNVs) in neurodevelopmental impairments among children with corpus callosum abnormalities (CCAs). We focused primarily on SLC6A3 associated mechanisms and aimed to delineate genotype-phenotype correlations in our cases. Methods From January 2021 to July 2023, 13 children with MRI-confirmed CCAs underwent chromosomal microarray analysis (CMA) for CNV detection. We performed bioinformatic analyses (Gene Ontology, STRING network) to identify neurodevelopmental genes within pathogenic CNVs, and clinical follow up assessed neurobehavioral outcomes. Results We identified pathogenic CNVs in 3/13 cases (23.08%). Specifically, Case 8 harbored a 43.05-Mb duplication (5p15.33p12) encompassing SLC6A3, a dopamine transporter gene linked to synaptic signaling. Interaction network analysis suggested that SLC6A3 was the most interconnected gene, providing evidence of its role in CCAs. Clinically, 84.6% of cases (11/13) exhibited psychomotor delay, while 15.4% of cases (2/13) developed seizure. Notably, we observed hearing impairment and psychomotor developmental delay in Case 8 with a SLC6A3 duplication, further suggesting dopaminergic dysregulation in callosal connectivity. Conclusion Our study suggests that SLC6A3 may represent a potential contributor to neurodevelopmental impairments in CCAs. Further, CMA-based CNV screening is critical for early intervention in high-risk children. These findings bridge genetic etiology with clinical phenotypes and offer insights into future targeted therapeutic strategies.https://doi.org/10.1186/s13039-025-00725-4
spellingShingle Shan-yu Liu
Wei Huang
Hui-lin Ou
Li Wang
Dan-dan Wang
Wei-he Tan
Qin She
Potential role of SLC6A3 in neurodevelopmental impairments associated with corpus callosum abnormalities: insights from CNV analysis and clinical phenotyping
Molecular Cytogenetics
title Potential role of SLC6A3 in neurodevelopmental impairments associated with corpus callosum abnormalities: insights from CNV analysis and clinical phenotyping
title_full Potential role of SLC6A3 in neurodevelopmental impairments associated with corpus callosum abnormalities: insights from CNV analysis and clinical phenotyping
title_fullStr Potential role of SLC6A3 in neurodevelopmental impairments associated with corpus callosum abnormalities: insights from CNV analysis and clinical phenotyping
title_full_unstemmed Potential role of SLC6A3 in neurodevelopmental impairments associated with corpus callosum abnormalities: insights from CNV analysis and clinical phenotyping
title_short Potential role of SLC6A3 in neurodevelopmental impairments associated with corpus callosum abnormalities: insights from CNV analysis and clinical phenotyping
title_sort potential role of slc6a3 in neurodevelopmental impairments associated with corpus callosum abnormalities insights from cnv analysis and clinical phenotyping
url https://doi.org/10.1186/s13039-025-00725-4
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