KREX2 is not essential for either procyclic or bloodstream form Trypanosoma brucei.

<h4>Background</h4>Most mitochondrial mRNAs in Trypanosoma brucei require RNA editing for maturation and translation. The edited RNAs primarily encode proteins of the oxidative phosphorylation system. These parasites undergo extensive changes in energy metabolism between the insect and b...

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Autores principales:	Jason Carnes, Nancy Lewis Ernst, Carey Wickham, Brian Panicucci, Kenneth Stuart
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/11bd609057d74d4ea05c24076fa1dc51
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spelling	oai:doaj.org-article:11bd609057d74d4ea05c24076fa1dc512021-11-18T07:25:05ZKREX2 is not essential for either procyclic or bloodstream form Trypanosoma brucei.1932-620310.1371/journal.pone.0033405https://doaj.org/article/11bd609057d74d4ea05c24076fa1dc512012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22438925/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Most mitochondrial mRNAs in Trypanosoma brucei require RNA editing for maturation and translation. The edited RNAs primarily encode proteins of the oxidative phosphorylation system. These parasites undergo extensive changes in energy metabolism between the insect and bloodstream stages which are mirrored by alterations in RNA editing. Two U-specific exonucleases, KREX1 and KREX2, are both present in protein complexes (editosomes) that catalyze RNA editing but the relative roles of each protein are not known.<h4>Methodology/principal findings</h4>The requirement for KREX2 for RNA editing in vivo was assessed in both procyclic (insect) and bloodstream form parasites by methods that use homologous recombination for gene elimination. These studies resulted in null mutant cells in which both alleles were eliminated. The viability of these cells demonstrates that KREX2 is not essential in either life cycle stage, despite certain defects in RNA editing in vivo. Furthermore, editosomes isolated from KREX2 null cells require KREX1 for in vitro U-specific exonuclease activity.<h4>Conclusions</h4>KREX2 is a U-specific exonuclease that is dispensable for RNA editing in vivo in T. brucei BFs and PFs. This result suggests that the U deletion activity, which is required for RNA editing, is primarily mediated in vivo by KREX1 which is normally found associated with only one type of editosome. The retention of the KREX2 gene implies a non-essential role or a role that is essential in other life cycle stages or conditions.Jason CarnesNancy Lewis ErnstCarey WickhamBrian PanicucciKenneth StuartPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 3, p e33405 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jason Carnes Nancy Lewis Ernst Carey Wickham Brian Panicucci Kenneth Stuart KREX2 is not essential for either procyclic or bloodstream form Trypanosoma brucei.
description	<h4>Background</h4>Most mitochondrial mRNAs in Trypanosoma brucei require RNA editing for maturation and translation. The edited RNAs primarily encode proteins of the oxidative phosphorylation system. These parasites undergo extensive changes in energy metabolism between the insect and bloodstream stages which are mirrored by alterations in RNA editing. Two U-specific exonucleases, KREX1 and KREX2, are both present in protein complexes (editosomes) that catalyze RNA editing but the relative roles of each protein are not known.<h4>Methodology/principal findings</h4>The requirement for KREX2 for RNA editing in vivo was assessed in both procyclic (insect) and bloodstream form parasites by methods that use homologous recombination for gene elimination. These studies resulted in null mutant cells in which both alleles were eliminated. The viability of these cells demonstrates that KREX2 is not essential in either life cycle stage, despite certain defects in RNA editing in vivo. Furthermore, editosomes isolated from KREX2 null cells require KREX1 for in vitro U-specific exonuclease activity.<h4>Conclusions</h4>KREX2 is a U-specific exonuclease that is dispensable for RNA editing in vivo in T. brucei BFs and PFs. This result suggests that the U deletion activity, which is required for RNA editing, is primarily mediated in vivo by KREX1 which is normally found associated with only one type of editosome. The retention of the KREX2 gene implies a non-essential role or a role that is essential in other life cycle stages or conditions.
format	article
author	Jason Carnes Nancy Lewis Ernst Carey Wickham Brian Panicucci Kenneth Stuart
author_facet	Jason Carnes Nancy Lewis Ernst Carey Wickham Brian Panicucci Kenneth Stuart
author_sort	Jason Carnes
title	KREX2 is not essential for either procyclic or bloodstream form Trypanosoma brucei.
title_short	KREX2 is not essential for either procyclic or bloodstream form Trypanosoma brucei.
title_full	KREX2 is not essential for either procyclic or bloodstream form Trypanosoma brucei.
title_fullStr	KREX2 is not essential for either procyclic or bloodstream form Trypanosoma brucei.
title_full_unstemmed	KREX2 is not essential for either procyclic or bloodstream form Trypanosoma brucei.
title_sort	krex2 is not essential for either procyclic or bloodstream form trypanosoma brucei.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/11bd609057d74d4ea05c24076fa1dc51
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KREX2 is not essential for either procyclic or bloodstream form Trypanosoma brucei.

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