A link between mitochondrial gene expression and life stage morphologies in Trypanosoma cruzi

Roger Ramirez-Barrios, Emily K. Susa, Clara M Smoniewski, Sean P. Faacks, Charles K. Liggett, Sara L. Zimmer

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


The protozoan Trypanosoma cruzi has a complicated dual-host life cycle, and starvation can trigger transition from the replicating insect stage to the mammalian-infectious nonreplicating insect stage (epimastigote to trypomastigote differentiation). Abundance of some mature RNAs derived from its mitochondrial genome increase during culture starvation of T. cruzi for unknown reasons. Here, we examine T. cruzi mitochondrial gene expression in the mammalian intracellular replicating life stage (amastigote), and uncover implications of starvation-induced changes in gene expression. Mitochondrial RNA levels in general were found to be lowest in actively replicating amastigotes. We discovered that mitochondrial respiration decreases during starvation in insect stage cells, despite the previously observed increases in mitochondrial mRNAs encoding electron transport chain (ETC) components. Surprisingly, T. cruzi epimastigotes in replete medium grow at normal rates when we genetically compromised their ability to perform insertion/deletion editing and thereby generate mature forms of some mitochondrial mRNAs. However, these cells, when starved, were impeded in the epimastigote to trypomastigote transition. Further, they experience a short-flagella phenotype that may also be linked to differentiation. We hypothesize a scenario where levels of mature RNA species or editing in the single T. cruzi mitochondrion are linked to differentiation by a yet-unknown signaling mechanism.

Original languageEnglish (US)
Pages (from-to)1003-1021
Number of pages19
JournalMolecular Microbiology
Issue number5
StatePublished - May 1 2020

Bibliographical note

Funding Information:
We acknowledge the laboratory of Dr. Esteban Serra for the pINDEX‐GW plasmid and transfection advice, and Dr. Martin Taylor, London School of Hygiene & Tropical Medicine for the pTcrRNA‐T7Tet plasmid. We thank Dr. Laurie Read for the T. brucei MRP2 & PRMT1 antibodies, RND antiserum, and the RND wild‐type overexpression cell line. This work was supported by American Heart Association Scientist Development Award 16SDG26420019 to SLZ. Tc T. brucei

Publisher Copyright:
© 2020 John Wiley & Sons Ltd


  • RNA editing
  • gene expression
  • life cycle stages
  • organelles
  • ribonuclease
  • trypanosomiasis

PubMed: MeSH publication types

  • Journal Article
  • Research Support, Non-U.S. Gov't


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