ArticleScientific reports2020
Casein kinase 1.2 over expression restores stress resistance to Leishmania donovani HSP23 null mutants.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- Essential role of glycogen synthase kinase 3 in regulating growth, drug response, and infectivity inAntimicrobial agents and chemotherapy · 2026Article
- Characterization of the dual functions of Leishmania CK1.2 in both the parasite and the macrophage.PloS one · 2026Article
- The paradigm of intracellular parasite survival and drug resistance in leishmanial parasite through genome plasticity and epigenetics: Perception and future perspective.Frontiers in cellular and infection microbiology · 2023Review
- Distinguishing functions of trypanosomatid protein kinases.Trends in parasitology · 2022Review
- Promastigote-to-Amastigote Conversion inPathogens (Basel, Switzerland) · 2022Review
- Identification of Resistance Determinants for a Promising Antileishmanial Oxaborole Series.Microorganisms · 2021Article
- Dangerous Duplicity: The Dual Functions of Casein Kinase 1 in Parasite Biology and Host Subversion.Frontiers in cellular and infection microbiology · 2021Review
- TheGenes · 2020Article
- Article
- Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leishmania donovani is a trypanosomatidic parasite and causes the lethal kala-azar fever, a neglected tropical disease. The Trypanosomatida are devoid of transcriptional gene regulation and rely on gene copy number variations and translational control for their adaption to changing conditions. To survive at mammalian tissue temperatures, L. donovani relies on the small heat shock protein HSP23, the loss of which renders the parasites stress sensitive and impairs their proliferation. Here, we analysed a spontaneous escape mutant with wild type-like in vitro growth. Further selection of this escape strains resulted in a complete reversion of the phenotype. Whole genome sequencing revealed a correlation between stress tolerance and the massive amplification of a six-gene cluster on chromosome 35, with further analysis showing over expression of the casein kinase 1.2 gene as responsible. In vitro phosphorylation experiments established both HSP23 and the related P23 co-chaperone as substrates and modulators of casein kinase 1.2, providing evidence for another crucial link between chaperones and signal transduction protein kinases in this early branching eukaryote.
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