Bipolar disorders · 2007
Human MIP synthase splice variants in bipolar disorder.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАПоддержка правительства СШАНазвание и аннотация: Перевод в очереди
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Shamir Alon, Shaltiel Galit, Mark Shirly, Bersudsky Yuly, Belmaker Robert H, Agam Galila
Аннотация
OBJECTIVES: Alternative splicing allows the production of multiple gene products with different functions from a given sequence, affecting cellular function control. Tissue-specific splicing is most prevalent in the brain. We therefore investigate whether splice variants contribute to complex psychiatric disorders. A database search suggested that the myo-inositol-1-phosphate (MIP) synthase gene, possibly involved in pathophysiology of bipolar disorder, has splice variants.
METHODS: Human RNA was purified from lymphocytes and postmortem brain. MIP synthase alternative splice variants were amplified using reverse transcription-polymerase chain reaction.
RESULTS: The bioinformatics finding was confirmed in both tissues. No difference in lymphocyte MIP synthase mRNA splice-variant levels was found between bipolar patients and controls. However, patients with family history of a major psychiatric disorder had significantly higher levels of the variant lacking exons 3 and 4 versus patients with no family history and controls.
CONCLUSIONS: As alternative splicing may be a mechanism by which the approximately 30,000 genes are amplified in mammalian brain, further studies with other candidate genes for psychiatric disorders are needed.
METHODS: Human RNA was purified from lymphocytes and postmortem brain. MIP synthase alternative splice variants were amplified using reverse transcription-polymerase chain reaction.
RESULTS: The bioinformatics finding was confirmed in both tissues. No difference in lymphocyte MIP synthase mRNA splice-variant levels was found between bipolar patients and controls. However, patients with family history of a major psychiatric disorder had significantly higher levels of the variant lacking exons 3 and 4 versus patients with no family history and controls.
CONCLUSIONS: As alternative splicing may be a mechanism by which the approximately 30,000 genes are amplified in mammalian brain, further studies with other candidate genes for psychiatric disorders are needed.