ArticlePLoS pathogens2018
Deletion of transketolase triggers a stringent metabolic response in promastigotes and loss of virulence in amastigotes of Leishmania mexicana.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
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- Cytosolic aldose metabolism contributes to progression from cirrhosis to hepatocarcinogenesis.Nature metabolism · 2023Article
- Amphotericin B resistance in Leishmania mexicana: Alterations to sterol metabolism and oxidative stress response.PLoS neglected tropical diseases · 2022Article
- Transcriptional Shift and Metabolic Adaptations duringMicroorganisms · 2022Article
- Profilin is involved in G1 to S phase progression and mitotic spindle orientation during Leishmania donovani cell division cycle.PloS one · 2022Article
- Histone acetylation regulates the expression of genes involved in worker reproduction in the ant Temnothorax rugatulus.BMC genomics · 2021Article
- Liquid Chromatography-Mass Spectrometry for Clinical Metabolomics: An Overview.Advances in experimental medicine and biology · 2021Article
- Suramin exposure alters cellular metabolism and mitochondrial energy production in African trypanosomes.The Journal of biological chemistry · 2020Article
- Article
- Mining for natural product antileishmanials in a fungal extract library.International journal for parasitology. Drugs and drug resistance · 2019Article
- Validation of Predicted Virulence Factors inToxins · 2019Article
- Untargeted metabolomics to understand the basis of phenotypic differences in amphotericin B-resistantWellcome open research · 2019Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Transketolase (TKT) is part of the non-oxidative branch of the pentose phosphate pathway (PPP). Here we describe the impact of removing this enzyme from the pathogenic protozoan Leishmania mexicana. Whereas the deletion had no obvious effect on cultured promastigote forms of the parasite, the Δtkt cells were not virulent in mice. Δtkt promastigotes were more susceptible to oxidative stress and various leishmanicidal drugs than wild-type, and metabolomics analysis revealed profound changes to metabolism in these cells. In addition to changes consistent with those directly related to the role of TKT in the PPP, central carbon metabolism was substantially decreased, the cells consumed significantly less glucose, flux through glycolysis diminished, and production of the main end products of metabolism was decreased. Only minor changes in RNA abundance from genes encoding enzymes in central carbon metabolism, however, were detected although fructose-1,6-bisphosphate aldolase activity was decreased two-fold in the knock-out cell line. We also showed that the dual localisation of TKT between cytosol and glycosomes is determined by the C-terminus of the enzyme and by engineering different variants of the enzyme we could alter its sub-cellular localisation. However, no effect on the overall flux of glucose was noted irrespective of whether the enzyme was found uniquely in either compartment, or in both.
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