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RNA Editing

A-to-I RNA editing is a post-transcriptional mechanism in which gnomically encoded Adenosine (A) is converted to Inosine (I) in the corresponding RNA, transcribed from the same locus.

This type of editing is catalyzed by ADAR enzymes, which target double-stranded RNA substrates.

The Inosine in the edited RNA is recognized by the cellular machineries as Guanosine (G). This changes the genomic code and increases the diversity of the transcriptome. The complexity of the molecular machinery that mediates A-to-I editing and the number of editing targets seems to increase from lower to higher organisms.

Moreover, ADAR mediated RNA editing has proven to be important for normal brain function, and diseases of the central nervous system, such as depression, epilepsy, schizophrenia and ALS have been linked to a deregulation of RNA editing.

In recent years, bioinformatics approaches were used to find editing sites and to estimate the prevalence of RNA editing in the human genome. Mismatch results of RNA transcripts alignment with the genome are considered editing candidates. The outcome of these approaches has revealed a few thousand new editing sites. Most of them were found in Alu repeats.

Alu repeats are very common in the human genome with more than million copies, and are characterized by low divergence. Thus, many genes may contain two similar and reversely oriented elements which are likely to form a double-stranded RNA structure, which is the preferred target for RNA editing. We assume that RNA editing is a much more common phenomenon, occurring in the human genome more frequently than has been shown up till now.

The upcoming high-throughput sequencing methods offer an increased coverage and depth of the sequenced transcriptome, which will allow us a better identification of the edited sites and characterization of the RNA editing phenomenon.