Qi Zhang: Translational Medical Center for Development and Disease, Shanghai Key Laboratory of Birth Defect Prevention and Control, Institute of Pediatrics, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, 201102, China.
Tingting Li: Translational Medical Center for Development and Disease, Shanghai Key Laboratory of Birth Defect Prevention and Control, Institute of Pediatrics, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, 201102, China.
Jia Lin: Translational Medical Center for Development and Disease, Shanghai Key Laboratory of Birth Defect Prevention and Control, Institute of Pediatrics, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, 201102, China.
Yinglan Zhang: Translational Medical Center for Development and Disease, Shanghai Key Laboratory of Birth Defect Prevention and Control, Institute of Pediatrics, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, 201102, China.
Fei Li: Translational Medical Center for Development and Disease, Shanghai Key Laboratory of Birth Defect Prevention and Control, Institute of Pediatrics, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, 201102, China.
Xudong Chen: Translational Medical Center for Development and Disease, Shanghai Key Laboratory of Birth Defect Prevention and Control, Institute of Pediatrics, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, 201102, China.
Xu Wang: Cancer Institute, Pancreatic Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
Qiang Li: Translational Medical Center for Development and Disease, Shanghai Key Laboratory of Birth Defect Prevention and Control, Institute of Pediatrics, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, 201102, China.
The cytoskeletal protein nde1 plays an important role in chromosome segregation, neural precursor differentiation, and neuronal migration. Clinical studies have shown that nde1 deficiency is associated with several neuropsychiatric disorders including autism. Here, we generated homologous deficiency zebrafish ( ) to elucidate the cellular molecular mechanisms behind it. exhibit increased neurological apoptotic responses at early infancy, enlarged ventricles, and shrank valvula cerebelli in adult brain tissue. Behavioral analysis revealed that displayed autism-like behavior traits such as increased locomotor activity and repetitive stereotype behaviors and impaired social and kin recognition behaviors. Furthermore, mRNA injection rescued apoptosis in early development, and minocycline treatment rescued impaired social behavior and overactive motor activity by inhibiting inflammatory cytokines. In this study, we revealed that homozygous deletion leads to abnormal neurological development with autism-related behavioral phenotypes and that inflammatory responses in the brain are an important molecular basis behind it.
