ArticleMolecular microbiology2015
LACK, a RACK1 ortholog, facilitates cytochrome c oxidase subunit expression to promote Leishmania major fitness.
Article in Molecular microbiology, 2015. 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, 15 citations in OpenAlex.
- Mitochondrial Localization and Abundance of Leishmania Cytochrome c Oxidase Subunit IV Is Maintained Following Loss of Mitochondrial Membrane Potential Associated With Mammalian Temperature.Molecular microbiology · 2026Article
- Investigation of viscerotropism-associated genes inFrontiers in microbiology · 2026Article
- UniqueFrontiers in cellular and infection microbiology · 2024Article
- Proteomic Analysis ofPathogens (Basel, Switzerland) · 2021Article
- Sterol 14-α-demethylase is vital for mitochondrial functions and stress tolerance in Leishmania major.PLoS pathogens · 2020Article
- Article
- Disruption of the Putative Ribosome-Binding Motif of a Scaffold Protein Impairs CytochromemSphere · 2019Article
- Sterol methyltransferase is required for optimal mitochondrial function and virulence in Leishmania major.Molecular microbiology · 2019Article
- WD40 Repeat Proteins: Signalling Scaffold with Diverse Functions.The protein journal · 2018Review
- Transcriptome Remodeling in Trypanosoma cruzi and Human Cells during Intracellular Infection.PLoS pathogens · 2016Article
- An analysis of phosphorylation sites in protein kinases fromBioinformation · 2016Article
- The genetics of Leishmania virulence.Medical microbiology and immunology · 2015Review
- Roles of Rack1 Proteins in Fungal Pathogenesis.BioMed research internationalReview
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Leishmania are kinetoplastid parasites that cause the sandfly-transmitted disease leishmaniasis. To maintain fitness throughout their infectious life cycle, Leishmania must undergo rapid metabolic adaptations to the dramatically distinct environments encountered during transition between sandfly and vertebrate hosts. We performed proteomic and immunoblot analyses of attenuated L. major strains deficient for LACK, the Leishmania ortholog of the mammalian receptor for activated c kinase (RACK1), that is important for parasite thermotolerance and virulence. This approach identified cytochrome c oxidase (LmCOX) subunit IV as a LACK-dependent fitness protein. Consistent with decreased levels of LmCOX subunit IV at mammalian temperature, and in amastigotes, LmCOX activity and mitochondrial function were also impaired in LACK-deficient L. major under these conditions. Importantly, overexpression of LmCOX subunit IV in LACK-deficient L. major restored thermotolerance and macrophage infectivity. Interestingly, overexpression of LmCOX subunit IV enhanced LmCOX subunit VI expression at mammalian temperature. Collectively, our data suggest LACK promotes Leishmania adaptation to the mammalian host environment by sustaining LmCOX subunit IV expression and hence energy metabolism in response to stress stimuli such as heat. These findings extend the repertoire of RACK1 protein utility to include a role in mitochondrial function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.