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Generation, Purification, and Characterization of Cell-invasive DISC1 Protein Species
Published on: August 30, 2012
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Disrupted-in-schizophrenia 1 (DISC1) regulates dysbindin function by enhancing its stability.
Seol-Ae Lee1, Seong-Mo Kim1, Bo Kyoung Suh1
1From the Department of Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.
The Journal of Biological Chemistry
|January 31, 2015
Summary
Dysbindin and DISC1 (Disrupted-in-Schizophrenia 1) proteins physically interact to stabilize dysbindin, which is crucial for neurite outgrowth in neuronal development. This interaction is vital for preventing schizophrenia-related developmental defects.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Dysbindin and DISC1 are implicated as susceptibility factors in schizophrenia.
- Both proteins play significant roles in neuronal development processes.
Purpose of the Study:
- To investigate the functional significance of the physical interaction between dysbindin and DISC1.
- To elucidate the role of this complex in neuronal development and stability.
Main Methods:
- Studied the physical interaction between dysbindin and DISC1.
- Assessed the impact of DISC1 knockdown and a specific DISC1 deletion mutant (DISC1(Δ403-504)) on dysbindin levels.
- Examined the effect of dysbindin and DISC1 coexpression on neurite outgrowth defects.
Main Results:
- DISC1 physically interacts with dysbindin, enhancing its stability by reducing ubiquitylation.
- Knockdown of DISC1 or expression of DISC1(Δ403-504) led to decreased endogenous dysbindin levels.
- Coexpression of dysbindin partially rescued neurite outgrowth defects caused by DISC1 knockdown.
Conclusions:
- Dysbindin and DISC1 form a physiologically functional complex essential for normal neurite outgrowth.
- This complex plays a critical role in maintaining dysbindin stability and neuronal development, potentially impacting schizophrenia pathogenesis.
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