ArticleMolecular microbiology2009
Amplification of an alternate transporter gene suppresses the avirulent phenotype of glucose transporter null mutants in Leishmania mexicana.
Article in Molecular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Glucose Transporters and Virulence inmSphere · 2018Article
- Leishmania mexicana can utilize amino acids as major carbon sources in macrophages but not in animal models.Molecular microbiology · 2018Article
- G-Quadruplex Identification in the Genome of Protozoan Parasites Points to Naphthalene Diimide Ligands as New Antiparasitic Agents.Journal of medicinal chemistry · 2018Article
- Metabolic reprogramming during purine stress in the protozoan pathogen Leishmania donovani.PLoS pathogens · 2014Article
- Induction of a stringent metabolic response in intracellular stages of Leishmania mexicana leads to increased dependence on mitochondrial metabolism.PLoS pathogens · 2014Article
- Plasmodial sugar transporters as anti-malarial drug targets and comparisons with other protozoa.Malaria journal · 2011Review
- Lysosomal degradation of Leishmania hexose and inositol transporters is regulated in a stage-, nutrient- and ubiquitin-dependent manner.International journal for parasitology · 2011Article
- Nutrient transport and pathogenesis in selected parasitic protozoa.Eukaryotic cell · 2011Review
- Remodeling of protein and mRNA expression in Leishmania mexicana induced by deletion of glucose transporter genes.Molecular and biochemical parasitology · 2011Article
- Leishmania UDP-sugar pyrophosphorylase: the missing link in galactose salvage?The Journal of biological chemistry · 2010Article
- Glucose transporters in parasitic protozoa.Methods in molecular biology (Clifton, N.J.) · 2010Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
A glucose transporter null mutant of the parasitic protozoan Leishmania mexicana, in which three linked glucose transporter genes have been deleted by targeted gene replacement, is unable to replicate as amastigote forms within phagolysomes of mammalian host macrophages and is avirulent. Spontaneous suppressors of the null mutant have been isolated that partially restore replication of parasites within macrophages. These suppressor mutants have amplified the gene for an alternative hexose transporter, the LmGT4 permease (previously called the D2 permease), on a circular extrachromosomal element, and they overexpress LmGT4 mRNA and protein. The suppressors have also regained the ability to transport hexoses, and they have reverted other phenotypes of the null mutant exhibiting enhanced resistance to oxidative killing, heat shock and starvation for nutrients, as well as augmented levels of the storage carbohydrate beta-mannan, increased cell size and increased growth as insect stage promastigotes compared with the unsuppressed mutant. Complementation of the null mutant with the LmGT4 gene on a multicopy episomal expression vector also reverted these phenotypes, confirming that suppression results from amplification of the LmGT4 gene. These results underscore the importance of hexose transporters for the infectious stage of the parasite life cycle.
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