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Schnurri-2 mutant mice are hypersensitive to stress and hyperactive
Tsuyoshi Takagi1, Wanzhu Jin, Kazuyoshi Taya
1Laboratory of Molecular Genetics, RIKEN Tsukuba Institute, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan.
Brain Research
|July 14, 2006
Summary
Schnurri-2 (Shn-2) is crucial for adult brain function. Mice lacking Shn-2 display heightened stress responses, anxiety, and altered locomotion, indicating its role in regulating behavior.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- The bone morphogenetic protein (BMP)/transforming growth factor-beta (TGF-beta)/activin superfamily influences nervous system development and adult brain function.
- The precise role of BMP/TGF-beta/activin signaling in modulating neuronal function is not fully understood.
- Schnurri (Shn) proteins are transcription factors involved in BMP signaling pathways, with Shn-2 known to regulate adipogenesis.
Purpose of the Study:
- To investigate the role of the transcription factor Schnurri-2 (Shn-2) in adult brain function and behavior.
- To determine the impact of Shn-2 deficiency on stress response, anxiety-like behavior, and locomotion.
Main Methods:
- Behavioral analysis of Shn-2 knockout (Shn-2(-/-)) mice compared to wild-type controls.
- Measurement of stress-induced corticosterone levels.
- Assessment of immediate early gene expression (e.g., c-Fos) in the brain.
Main Results:
- Shn-2(-/-) mice exhibited increased hypersensitivity to stress and anxiety-like behavior.
- Stress-induced corticosterone levels were significantly elevated in Shn-2(-/-) mice.
- Shn-2(-/-) mice showed increased activity in familiar environments and decreased basal and stress-induced expression of immediate early genes like c-Fos.
Conclusions:
- Shn-2 plays a critical role in regulating anxiety-like behavior and stress responses in adult mice.
- Shn-2 influences locomotion and the expression of immediate early genes in the brain.
- These findings highlight Shn-2 as a key molecular player in adult brain function and behavior.

