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Forebrain excitatory neuron-specific SENP2 knockout mouse displays hyperactivity, impaired learning and memory, and
Dehua Huang1, Huiqing Liu1, Aoxue Zhu1
1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai, 200025, China.
Molecular Brain
|April 16, 2020
Summary
Sentrin/SUMO-specific protease 2 (SENP2) removal in mice caused hyperactivity and anxiety-like behaviors. This study reveals SENP2
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Sentrin/SUMO-specific protease 2 (SENP2) is crucial for SUMO protein regulation and highly expressed in the central nervous system (CNS).
- Previous research linked SENP2 to development, metabolism, and epilepsy, but its specific CNS functions remain unclear.
Purpose of the Study:
- To investigate the role of SENP2 in the CNS and its potential contribution to neuropathology.
- To establish a mouse model for studying SENP2's neurological functions.
Main Methods:
- Generated SENP2 conditional knockout mice by crossing floxed SENP2 mice with CaMKIIα-Cre transgenic mice.
- Conducted behavioral tests to assess neurological functions.
- Utilized RNA sequencing (RNA-seq) to analyze gene expression changes.
Main Results:
- SENP2 ablation in mice led to increased locomotor activity and anxiolytic-like behaviors.
- Mice lacking SENP2 exhibited deficits in spatial working memory and fear-associated learning.
- RNA-seq identified differential gene expression related to locomotion, learning, and memory.
Conclusions:
- SENP2 plays a significant role in regulating emotions and cognitive functions within the CNS.
- The developed SENP2 conditional knockout mouse model offers a valuable tool for exploring mechanisms of neuropsychiatric disorders.
