Key result
Silencing TbRGG1 reduces edited mRNAs and reveals a novel multiprotein complex in Trypanosoma brucei.
Why the study?
The role of TbRGG1 protein and its associated multiprotein complex in kinetoplastid mitochondrial RNA editing and metabolism was not fully understood.
TbRGG1 is essential for cell growth and plays a key role in stabilizing edited RNAs or editing efficiency in Trypanosoma brucei.
TbRGG1 knockdown impairs trypanosome RNA editing; leaves open its viability as a selective antiparasitic target pending in vivo validation.
The uridine insertion/deletion RNA editing of kinetoplastid mitochondrial transcripts is performed by complex machinery involving a number of proteins and multiple protein complexes. Here we describe the effect of silencing of TbRGG1 gene by RNA interference on RNA editing in procyclic stage of Trypanosoma brucei. TbRGG1 is an essential protein for cell growth, the absence of which results in an overall decline of edited mRNAs, while the levels of never-edited RNAs remain unaltered. Repression of TbRGG1 expression has no effect on the 20S editosome and MRP1/2 complex. TAP-tag purification of TbRGG1 coisolated a novel multiprotein complex, and its association was further verified by TAP-tag analyses of two other components of the complex. TbRGG1 interaction with this complex appears to be mediated by RNA. Our results suggest that the TbRGG1 protein functions in stabilizing edited RNAs or editing efficiency and that the associated novel complex may have a role in mitochondrial RNA metabolism. We provisionally name it putative mitochondrial RNA-binding complex 1 (put-MRB complex 1).
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Hashimi et al. (2008) studied this question. Silencing of TbRGG1 gene by RNA interference was evaluated on RNA editing and cell growth. Silencing of the essential TbRGG1 gene in Trypanosoma brucei resulted in an overall decline of edited mRNAs and revealed its association with a novel multiprotein complex.
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