ArticleScientific reports2016
Disclosing the essentiality of ribose-5-phosphate isomerase B in Trypanosomatids.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 33 citations in OpenAlex.
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- Toward Chemical Validation of Leishmania infantum Ribose 5-Phosphate Isomerase as a Drug Target.Antimicrobial agents and chemotherapy · 2021Article
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- Murine infection with bioluminescent Leishmania infantum axenic amastigotes applied to drug discovery.Scientific reports · 2019Article
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- Deletion of transketolase triggers a stringent metabolic response in promastigotes and loss of virulence in amastigotes of Leishmania mexicana.PLoS pathogens · 2018Article
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- Essential multimeric enzymes in kinetoplastid parasites: A host of potentially druggable protein-protein interactions.PLoS neglected tropical diseases · 2017Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Ribose-5-phosphate isomerase (RPI) belongs to the non-oxidative branch of the pentose phosphate pathway, catalysing the inter-conversion of D-ribose-5-phosphate and D-ribulose-5-phosphate. Trypanosomatids encode a type B RPI, whereas humans have a structurally unrelated type A, making RPIB worthy of exploration as a potential drug target. Null mutant generation in Leishmania infantum was only possible when an episomal copy of RPIB gene was provided, and the latter was retained both in vitro and in vivo in the absence of drug pressure. This suggests the gene is essential for parasite survival. Importantly, the inability to remove the second allele of RPIB gene in sKO mutants complemented with an episomal copy of RPIB carrying a mutation that abolishes isomerase activity suggests the essentiality is due to its metabolic function. In vitro, sKO promastigotes exhibited no defect in growth, metacyclogenesis or macrophage infection, however, an impairment in intracellular amastigotes' replication was observed. Additionally, mice infected with sKO mutants rescued by RPIB complementation had a reduced parasite burden in the liver. Likewise, Trypanosoma brucei is resistant to complete RPIB gene removal and mice infected with sKO mutants showed prolonged survival upon infection. Taken together our results genetically validate RPIB as a potential drug target in trypanosomatids.
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