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Generation and initial characterization of mice lacking full-length BAI3 (ADGRB3) expression
Fu Hung Shiu1,2, Jennifer C Wong1, Debanjan Bhattacharya3
1Department of Human Genetics, Emory University School of Medicine, Atlanta, Georgia, USA.
Basic & Clinical Pharmacology & Toxicology
|June 20, 2023
Summary
Researchers generated a mouse model lacking full-length brain-specific angiogenesis inhibitor 3 (ADGRB3). These mice showed reduced weight and social deficits, aiding ADGRB3 function studies in neurological disorders and cancer.
Area of Science:
- Neuroscience
- Genetics
- Molecular Biology
Background:
- Brain-specific angiogenesis inhibitor 3 (ADGRB3/BAI3) is an adhesion G protein-coupled receptor highly expressed in the brain.
- ADGRB3 plays a role in synaptogenesis and synapse maintenance, with implications in schizophrenia and epilepsy.
- Somatic mutations in ADGRB3 are linked to various cancer types.
Purpose of the Study:
- To generate and characterize a mouse model for studying the in vivo physiological role of ADGRB3.
- To investigate the impact of ADGRB3 deficiency on brain and body development, and behavior.
- To provide a tool for exploring ADGRB3's function in both central nervous system and non-central nervous system contexts, including cancer development.
Main Methods:
- CRISPR/Cas9 gene editing was used to create a mouse line with a 7-base pair deletion in Adgrb3 exon 10.
- Western blot analysis confirmed the absence of full-length ADGRB3 in homozygous mutants (Adgrb3∆7/∆7).
- Phenotypic analyses included assessments of body and brain weight, social interaction, locomotor function, olfaction, anxiety, and prepulse inhibition.
Main Results:
- Homozygous Adgrb3∆7/∆7 mutant mice were viable and bred normally, exhibiting Mendelian ratios.
- Mutant mice displayed significantly reduced brain and body weights compared to wild-type littermates.
- Deficits in social interaction were observed in mutant mice, while locomotor function, olfaction, anxiety, and prepulse inhibition remained comparable across genotypes.
Conclusions:
- The generated Adgrb3∆7/∆7 mouse model effectively lacks full-length ADGRB3 expression and is suitable for studying its physiological roles.
- ADGRB3 deficiency in mice leads to developmental and behavioral alterations, including reduced weight and impaired social interaction.
- This mouse model serves as a valuable resource for future research into ADGRB3's involvement in neurological disorders, non-CNS functions, and tumorigenesis.
