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Background  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.    Methodology/Principal Findings  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.    Conclusions  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.

KREX2 Is Not Essential for Either Procyclic or Bloodstream Form Trypanosoma brucei