RNA Editing in African Trypanosomes: A U-ser’s G-U-ide

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RNA Metabolism in Trypanosomes

Part of the book series: Nucleic Acids and Molecular Biology ((NUCLEIC,volume 28))

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Abstract

Of the chemical repertoire of RNA processing pathways, one reaction cycle stands out due to its idiosyncratic features. The process has evolved within the mitochondria of only one clad of organisms, the kinetoplastid protozoa (Excavata, Euglenozoa), which include the African trypanosome, the causative agent of slee** sickness. The process can be categorized as an RNA editing-type reaction. It is characterized by the insertion and/or deletion of uridine nucleotides into otherwise nontranslatable mRNAs. Kinetoplastid RNA editing relies on an exclusive class of trans-acting, small noncoding RNA molecules known as guide RNAs. Furthermore, a unique molecular machinery, the editosome, catalyzes the process. Editosomes represent high-molecular-mass multienzyme assemblies that provide a catalytic surface for the individual steps of the editing reaction cycle. Here I review the current mechanistic model of the editing reaction and I summarize the molecular components and accessory factors of the editosome machinery. Special emphasis is put on the recent discovery of the molecular structure of the editing complex, which allows a first correlation of structural features with functional characteristics.

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Acknowledgements

This work was supported by the Howard Hughes Medical Institute (HHMI), the German Research Foundation (DFG), and the Dr. Illing Foundation. The author would like to thank all members of the laboratory (past and present) for their contributions and their enthusiasm. Mike Roskope is acknowledged for discussions and comments on the manuscript. Holger Stark, Monika M. Golas, and Bjoern Sander are thanked for a productive cooperation.

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Correspondence to H. Ulrich Göringer .

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Göringer, H.U. (2012). RNA Editing in African Trypanosomes: A U-ser’s G-U-ide. In: Bindereif, A. (eds) RNA Metabolism in Trypanosomes. Nucleic Acids and Molecular Biology, vol 28. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-28687-2_7

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