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RNA editing by adenosine (A) to inosine (I) modification generates RNA and protein diversity in higher eukaryotes selectively altering coding and non-coding sequences in nuclear transcripts. The enzymes responsible for A-to-I editing, the adenosine deaminases acting on RNA (ADARs), are ubiquitously expressed in mammals and specifically recognize partially double-stranded (ds) RNA structures where they modify individual adenosines depending on the local structure and sequence environment. Long extended dsRNAs undergo massive editing, whereas RNA duplex structures with bulges and loops are subject to site-selective editing, as observed in several neurotransmitter receptor mRNAs ensuing single amino acid substitutions.

The adenosine deaminases acting on RNA (ADARs) specifically target single nucleotides for editing within the partially double-stranded pre-mRNAs of their substrates, such as neuronal glutamate and serotonin receptor transcripts. Since inosine is read as guanosine by the translation machinery, A-to-I editing often leads to codon changes that result in the alteration of protein function. It can also create or destroy pre-mRNA splice signals or lead to alterations in RNA secondary structure.

The deficiency or misregul ation of A-to-I RNA editing has been implicated in the etiology of neurological diseases, such as epilepsy, amyotrophic lateral sclerosis (ALS), and depression in mammals and it has been shown that a loss of A-to-I editing following the genetic inactivation of ADARs in mammals, as well as flies and the worm, results in behavioral or neurological dysfunctions or embryonic lethality (ADAR1).


RNA editing by adenosine (A) to inosine (I) modification generates RNA and protein diversity in higher eukaryotes selectively altering coding and non-coding sequences in nuclear transcripts. The enzymes responsible for A-to-I editing, the adenosine deaminases acting on RNA (ADARs), are ubiquitously expressed in mammals and specifically recognize partially double-stranded (ds) RNA structures where they modify individual adenosines depending on the local structure and sequence environment. Long extended dsRNAs undergo massive editing, whereas RNA duplex structures with bulges and loops are subject to site-selective editing, as observed in several neurotransmitter receptor mRNAs ensuing single amino acid substitutions. The adenosine deaminases acting on RNA (ADARs) specifically target single nucleotides for editing within the partially double-stranded pre-mRNAs of their substrates, such as neuronal glutamate and serotonin receptor transcripts. Since inosine is read as guanosine by the translation machinery, A-to-I editing often leads to codon changes that result in the alteration of protein function. It can also create or destroy pre-mRNA splice signals or lead to alterations in RNA secondary structure. The deficiency or misregul ation of A-to-I RNA editing has been implicated in the etiology of neurological diseases, such as epilepsy, amyotrophic lateral sclerosis (ALS), and depression in mammals and it has been shown that a loss of A-to-I editing following the genetic inactivation of ADARs in mammals, as well as flies and the worm, results in behavioral or neurological dysfunctions or embryonic lethality (ADAR1).		A - to - I RNA Editing Blog Forum

		*Monday, February 18, 2008* RNA-mediated epigenetic programming of a genome-rearrangement pathway A demonstration that DNA or RNA templates can orchestrate these genome rearrangements in Oxytricha Nature Link posted by RNA Editing lab-LU at 3:09 PM 0 comments --------------------------------------------------------------------------- Friday, February 23, 2007 RNA editing of micro RNAs More intriguing evidence that miRNAs might be important targets of the A-to-I RNA editing machinery. This study highlights the notion that for elucidating the function of miRNAs it is important to consider the possibility that the primary miRNA transcript may be modified altering the molecule's target spectrum. Link to Science Magazine Posted by RNA Editing lab-LU at 2:51 PM 0 comments --------------------------------------------------------------------------- Thursday, Feburary 15, 2007 Splicing and the Evolution of Proteins in Mammals regarding the dual role of exon sequences in encoding protein sequence and regulating splicing. A similar problem that also affects exons of edited genes where the coding sequence might also participate in RNA secondary structures that regulate editing. Link to PLoS Biology Author Summary: While information for pre-mRNA splicing is largely within the intron sequences of genes, parts of the exons near the intron–exon boundary can, for example, function as splice enhancer elements. In principle, then, these parts of exons have two functions: to specify the amino acids of the resulting protein and to enable the correct removal of introns. What impact might this have on a gene's evolution? The authors show that near intron–exon boundaries, amino acid usage is biased towards nucleotides involved in splice control. Moreover, these parts of genes evolve especially slowly. They estimate that a gene with many exons would evolve at under half the rate of the same gene with no introns, simply owing to the need to specify where to remove introns. Likewise, genes that have lost their introns evolve especially fast near the former intron's location. Thus, human proteins may not be as optimised as they could be, as their sequence is serving two conflicting roles. posted by RNA Editing lab-LU at 2:36 PM 0 comments -------------------------------------------------------------------------- Thursday, Feburary 15, 2007 PLoS ONE is launched A new journal under the open acces model that does things differently. Have a look. posted by RNA Editing lab-LU at 2:31 PM 0 comments -------------------------------------------------------------------------- Wednesday, November 29, 2006 An intriguing paper on the "Variability and memory of protein levels in human cells". ABSTRA CT Might have important implications for 'phenotypic diversity/heterogeneity within populations of cells'. posted by RNA Editing lab-LU at 10:46 AM 1 comments --------------------------------------------------------------------------- See our ARCHIVES* for past Posts*

Adenosine Deaminases Acting on RNA

This website is meant as an information resource for the A-to-I RNA editing community and anybody interested in adenosine deamination RNA editing. It will be continuously updated and improved. If you know of any A-to-I RNA editing lab information not listed here or have comments or suggestions regarding this website, please contact me

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	last updated May 2008