Abstract
BackgroundAdenosine to inosine (A-to-I) RNA-editing is an essential post-transcriptional mechanism that occurs in numerous sites in the human transcriptome, mainly within Alu repeats. It has been shown to have consistent levels of editing across individuals in a few targets in the human brain and altered in several human pathologies. However, the variability across human individuals of editing levels in other tissues has not been studied so far.ResultsHere, we analyzed 32 skin samples, looking at A-to-I editing level in three genes within coding sequences and in the Alu repeats of six different genes. We observed highly consistent editing levels across different individuals as well as across tissues, not only in coding targets but, surprisingly, also in the non evolutionary conserved Alu repeats.ConclusionsOur findings suggest that A-to-I RNA-editing of Alu elements is a tightly regulated process and, as such, might have been recruited in the course of primate evolution for post-transcriptional regulatory mechanisms.
Highlights
Adenosine to inosine (A-to-I) RNA-editing is an essential post-transcriptional mechanism that occurs in numerous sites in the human transcriptome, mainly within Alu repeats
Editing levels are consistent among skin samples of human individuals both in coding and non-coding sequences In healthy brain tissue, editing levels for the recoding sites within the glutamate receptor are highly uniform across individuals [10,12,24]
Mice ADAR1 or ADAR2 knockout die in-utero or shortly after birth, RNA editing is implicated as relevant to the skin in humans by the observation that mutations in ADAR1 lead to Dyschromatosis symmetrica hereditaria [27], a pigmenting genodermatosis with an autosomal dominant inheritance reported predominantly in Japanese and Chinese individuals [28]
Summary
Adenosine to inosine (A-to-I) RNA-editing is an essential post-transcriptional mechanism that occurs in numerous sites in the human transcriptome, mainly within Alu repeats. It has been shown to have consistent levels of editing across individuals in a few targets in the human brain and altered in several human pathologies. The variability across human individuals of editing levels in other tissues has not been studied so far. Site-selective adenosine to inosine (A-to-I) RNA-editing is an essential post-transcriptional mechanism for expanding the proteomic repertoire. It is carried out by members of the double-stranded RNA-specific ADAR family predominantly acting on precursor messenger RNAs [1]. A-to-I editing affects numerous sites in the human transcriptome, most of which are located in Alu elements
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