Tail characteristics of Trypanosoma brucei mitochondrial transcripts are developmentally altered in a transcript-specific manner

Vahid H. Gazestani, Marshall Hampton, Aubie K. Shaw, Reza Salavati, Sara L. Zimmer

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

The intricate life cycle of Trypanosoma brucei requires extensive regulation of gene expression levels of the mtRNAs for adaptation. Post-transcriptional gene regulatory programs, including unencoded mtRNA 3′ tail additions, potentially play major roles in this adaptation process. Intriguingly, T. brucei mitochondrial transcripts possess two distinct unencoded 3′ tails, each with a differing functional role; i.e., while one type is implicated in RNA stability (in-tails), the other type appears associated with translation (ex-tails). We examined the degree to which tail characteristics differ among cytochrome c oxidase subunits I and III (CO1 and CO3), and NADH dehydrogenase subunit 1 (ND1) transcripts, and to what extent these characteristics differ developmentally. We found that CO1, CO3 and ND1 transcripts possess longer in-tails in the mammalian life stage. By mathematically modelling states of in-tail and ex-tail addition, we determined that the typical length at which an in-tail is extended to become an ex-tail differs by transcript and, in the case of ND1, by life stage. To the best of our knowledge, we provide the first evidence that developmental differences exist in tail length distributions of mtRNAs, underscoring the potential involvement of in-tail and ex-tail populations in mitochondrial post-transcriptional regulation mechanisms.

Original languageEnglish (US)
Pages (from-to)179-189
Number of pages11
JournalInternational Journal for Parasitology
Volume48
Issue number2
DOIs
StatePublished - Feb 2018

Bibliographical note

Funding Information:
This study was supported through University of Minnesota , USA laboratory start-up funds to SLZ and Natural Sciences and Engineering Research Council of Canada ( NSERC ) grant # 328186 to RS. VHG is supported by a Canadian Institutes of Health Research Systems Biology Fellowship. The Minnesota Supercomputing Institute (MSI) at the University of Minnesota provided resources that contributed to the research results reported within this paper. We wish to thank Rebecca A. Madden for her support in cloning qPCR amplicons for Sanger sequencing. The authors declare no competing financial interests.

Funding Information:
This study was supported through University of Minnesota, USA laboratory start-up funds to SLZ and Natural Sciences and Engineering Research Council of Canada (NSERC) grant #328186 to RS. VHG is supported by a Canadian Institutes of Health Research Systems Biology Fellowship. The Minnesota Supercomputing Institute (MSI) at the University of Minnesota provided resources that contributed to the research results reported within this paper. We wish to thank Rebecca A. Madden for her support in cloning qPCR amplicons for Sanger sequencing. The authors declare no competing financial interests.

Publisher Copyright:
© 2017 Australian Society for Parasitology

Keywords

  • Hidden Markov modelling
  • Mitochondrion
  • Polyadenylation
  • RNA tail
  • Trypanosoma
  • Uridylation

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