Gene expression to mitochondrial metabolism: Variability among cultured Trypanosoma cruzi strains

Murat C. Kalem, Evgeny S. Gerasimov, Pamela K. Vu, Sara L Zimmer

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3 Scopus citations

Abstract

The insect-transmitted protozoan parasite Trypanosoma cruzi experiences changes in nutrient availability and rate of flux through different metabolic pathways across its life cycle. The species encompasses much genetic diversity of both the nuclear and mitochondrial genomes among isolated strains. The genetic or expression variation of both genomes are likely to impact metabolic responses to environmental stimuli, and even steady state metabolic function, among strains. To begin formal characterization these differences, we compared aspects of metabolism between genetically similar strains CL Brener and Tulahuen with less similar Esmeraldo and Sylvio X10 strains in a culture environment. Epimastigotes of all strains took up glucose at similar rates. However, the degree of medium acidification that could be observed when glucose was absent from the medium varied by strain, indicating potential differences in excreted metabolic byproducts. Our main focus was differences related to electron transport chain function. We observed differences in ATP-coupled respiration and maximal respiratory capacity, mitochondrial membrane potential, and mitochondrial morphology between strains, despite the fact that abundances of two nuclear-encoded proteins of the electron transport chain are similar between strains. RNA sequencing reveals strain-specific differences in abundances of mRNAs encoding proteins of the respiratory chain but also other metabolic processes. From these differences in metabolism and mitochondrial phenotypes we have generated tentative models for the differential metabolic fluxes or differences in gene expression that may underlie these results.

Original languageEnglish (US)
Article numbere0197983.
JournalPloS one
Volume13
Issue number5
DOIs
StatePublished - May 2018

Bibliographical note

Funding Information:
This study was supported through a Whiteside Institute for Clinical Research (MN, USA) grant to SLZ, and the American Heart Association [grant number 16SDG26420019 to SLZ]. PKV was supported by the National institutes of Health - National Institute of General Medical Sciences [IMSD GM086669]. The funders had no role in The authors thank Emily Susa and Dr. Roger Ramirez-Barrios for technical support and Dr. Richard Melvin for critical reading of the manuscript.

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