The human genome mostly consists of DNA that does not encode for protein. Although originally thought to represent evolutionary ‘junk,’ it has been shown that much of the junk DNA in the human genome is actively transcribed to RNA in a highly regulated, tissue-specific manner. Following this insight, ...
The human genome mostly consists of DNA that does not encode for protein. Although originally thought to represent evolutionary ‘junk,’ it has been shown that much of the junk DNA in the human genome is actively transcribed to RNA in a highly regulated, tissue-specific manner. Following this insight, non-coding RNAs (ncRNAs) were demonstrated to be fundamental to many intracellular processes, such as targeting transcription factors to their binding sites, initiating chromatin remodeling, blocking transcription or translation of other genes both in cis and trans, and a variety of other functions that are still being uncovered. Perhaps not surprisingly, studies quickly followed showing that disruption of ncRNA biogenesis can lead to molecular and cellular defects. Recently, ncRNAs have been demonstrated to be abnormal in the brains of patients with common neurodevelopmental disorders and their animal models, such as autism, schizophrenia, and bipolar disorder. These diseases were previously known to have a significant hereditary component, but their genomic etiology is complex and has remained poorly understood. Emerging research into underlying ncRNA problems in these disorders has the potential to reconcile their known heritability with their genomic and phenotypic heterogeneity, and hopefully unveil novel genomic pathologic mechanisms that can ultimately lead to new molecular therapeutics. In this Research Topic, we will present a broad array of reviews and new findings in this emerging and critically important area of neurosciences research.
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