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The Journal of Neuroscience, June 1, 2005, 25(22):5376-5381; doi:10.1523/JNEUROSCI.0766-05.2005

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BRIEF COMMUNICATION
DNA Methylation Status of SOX10 Correlates with Its Downregulation and Oligodendrocyte Dysfunction in Schizophrenia

Kazuya Iwamoto,¹ Miki Bundo,¹ Kazuo Yamada,² Hitomi Takao,² Yoshimi Iwayama-Shigeno,² Takeo Yoshikawa,² and Tadafumi Kato¹

¹Laboratory for Molecular Dynamics of Mental Disorders, and ²Laboratory for Molecular Psychiatry, RIKEN Brain Science Institute, Saitama 351-0198, Japan

Downregulation of oligodendrocyte-related genes, referred to as oligodendrocyte dysfunction, in schizophrenia has been revealed by DNA microarray studies. Because oligodendrocyte-specific transcription factors regulate the differentiation of oligodendrocytes, genes encoding them are prime candidates for oligodendrocyte dysfunction in schizophrenia. We found that the cytosine-guanine dinucleotide (CpG) island of sex-determining region Y-box containing gene 10 (SOX10), an oligodendrocyte-specific transcription factor, tended to be highly methylated in brains of patients with schizophrenia, correlated with reduced expression of SOX10. We also found that DNA methylation status of SOX10 also was associated with other oligodendrocyte gene expressions in schizophrenia. This may be specific to SOX10, because the CpG island of OLIG2, which encodes another oligodendrocyte-specific transcription factor, was rarely methylated in brains, and the methylation status of myelin-associated oligodendrocytic basic protein, which encodes structural protein in oligodendrocytes, did not account for their expressions or other oligodendrocyte gene expressions. Therefore, DNA methylation status of the SOX10 CpG island could be an epigenetic sign of oligodendrocyte dysfunction in schizophrenia.

Key words: oligodendrocyte; postmortem; schizophrenia; DNA methylation; epigenetics; SOX10

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Received Feb 25, 2005; revised April 18, 2005; accepted April 26, 2005.

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