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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.

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|June 20, 2023
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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.

Keywords:
ADGRB3AGPCRBAI3Schizophreniaseizure

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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.