Key result
Depletion of the Trypanosoma brucei MTR4-like protein caused growth arrest and defects in 5.8S rRNA processing, suggesting conserved polyadenylation-dependent nuclear rRNA quality control.
This study demonstrates that polyadenylation-dependent nuclear rRNA quality control is conserved in eukaryotic evolution, although the TRAMP complex interactions may differ in trypanosomes.
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Supports evolutionary conservation of rRNA quality control in trypanosomes; leaves open whether TRAMP interactions are universal across eukaryotes.
The yeast putative RNA helicase Mtr4p is implicated in exosome-mediated RNA quality control in the nucleus, interacts with the exosome, and is found in the 'TRAMP' complex with a yeast nuclear poly(A) polymerase (Trf4p/Pap2p or Trf5p) and a putative RNA-binding protein, Air1p or Air2p. Depletion of the Trypanosoma brucei MTR4-like protein TbMTR4 caused growth arrest and defects in 5.8S rRNA processing similar to those seen after depletion of the exosome. TbNPAPL, a nuclear protein which is a putative homolog of Trf4p/Pap2p, was required for normal cell growth. Depletion of MTR4 resulted in the accumulation of polyadenylated rRNA precursors, while depletion of TbNPAPL had little effect. These results suggest that polyadenylation-dependent nuclear rRNA quality control is conserved in eukaryotic evolution. In contrast, there was no evidence for a trypanosome TRAMP complex since no stable interactions between TbMTR4 and the exosome, TbNPAPL or RNA-binding proteins were detected.
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Cristodero et al. (2007) studied this question. Depletion of TbMTR4 was evaluated on Cell growth and rRNA processing. Depletion of the Trypanosoma brucei MTR4-like protein caused growth arrest and defects in 5.8S rRNA processing, suggesting conserved polyadenylation-dependent nuclear rRNA quality control.
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