This study investigates the role of EBP1 in cerebellar development and its association with schizophrenia-like behaviors. Using Ebp1 conditional Knockout (CKO) mice with CNS-specific deletion, researchers observed reduced cerebellar volume, Purkinje cell loss, and abnormal dendritic development. These structural deficits led to motor impairments and schizophrenia-like behaviors. Mechanistically, Ebp1 deficiency resulted in upregulation of Fbxw7, leading to degradation of PTF1A, a transcription factor critical for Purkinje cell development. Reintroduction of wild-type EBP1, but not the schizophrenia-associated E183Ter mutant, restored cerebellar architecture and behavioral phenotypes.
Ebp1 deficiency in the CNS leads to cerebellar structural abnormalities and schizophrenia-like behaviors, highlighting its critical role in neurodevelopment and potential involvement in neuropsychiatric disorders.
CNS-specific Ebp1 conditional Knockout (CKO) mice generated using Cre-loxP system to study the effects of Ebp1 deficiency on cerebellar development and behavior.
Neurodevelopment, Schizophrenia, Cerebellar dysfunction, Purkinje cells, Epigenetic regulation
Conditional Knockout, Cre-loxP system, CNS-specific gene deletion, Behavioral phenotyping
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
