Editor meets silencer: crosstalk between RNA editing and RNA interference

Abstract

Adenosine to inosine (A→I) RNA editing is catalysed by ADAR (adenosine deaminases acting on RNA) proteins. Three mammalian ADAR genes (ADAR1–3), the products of which have common functional domains, have been identified. Protein-coding sequences of a limited number of genes, such as the glutamate receptor GluR2 and serotonin receptor 2C, are edited, which results in dramatic alterations of protein functions. Deficiencies in the A→I RNA editing mechanism cause human diseases and pathophysiologies. Recent bioinformatics studies identified numerous A→I RNA editing sites genome wide in Alu and long interspersed element (LINE) repetitive RNA sequences located in introns and untranslated regions, but identified only a few sites in protein-coding exons. The biogenesis of certain microRNAs is regulated by the editing of their precursors. A→I RNA editing and RNA-interference mechanisms seem to interact and compete for common substrate double-stranded RNAs.