ArticleEukaryotic cell2006
A Mitogen-activated protein kinase controls differentiation of bloodstream forms of Trypanosoma brucei.
Article in Eukaryotic cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 74 citations in OpenAlex.
- Pathogenicity and virulence of African trypanosomes: From laboratory models to clinically relevant hosts.Virulence · 2023Review
- Piplartine-Inspired 3,4,5-Trimethoxycinnamates: Trypanocidal, Mechanism of Action, and In Silico Evaluation.Molecules (Basel, Switzerland) · 2023Article
- An Ebola,Computational and structural biotechnology journal · 2021Article
- Culturing and Transfection of Pleomorphic Trypanosoma brucei.Methods in molecular biology (Clifton, N.J.) · 2020Article
- Non-linear hierarchy of the quorum sensing signalling pathway in bloodstream form African trypanosomes.PLoS pathogens · 2018Article
- Emerging challenges in understanding trypanosome antigenic variation.Emerging topics in life sciences · 2017Article
- The Cytological Events and Molecular Control of Life Cycle Development of Trypanosoma brucei in the Mammalian Bloodstream.Pathogens (Basel, Switzerland) · 2017Review
- Extracellular-signal regulated kinase 8 of Trypanosoma brucei uniquely phosphorylates its proliferating cell nuclear antigen homolog and reveals exploitable properties.Cell cycle (Georgetown, Tex.) · 2016Article
- A new approach to chemotherapy: drug-induced differentiation kills African trypanosomes.Scientific reports · 2016Article
- Quantitative Proteomics Uncovers Novel Factors Involved in Developmental Differentiation of Trypanosoma brucei.PLoS pathogens · 2016Article
- The within-host dynamics of African trypanosome infections.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Review
- Cancer in the parasitic protozoans Trypanosoma brucei and Toxoplasma gondii.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Assembling the components of the quorum sensing pathway in African trypanosomes.Molecular microbiology · 2015Review
- Quantitative proteomic and phosphoproteomic analysis of Trypanosoma cruzi amastigogenesis.Molecular & cellular proteomics : MCP · 2014Article
- The design and synthesis of potent and selective inhibitors of Trypanosoma brucei glycogen synthase kinase 3 for the treatment of human african trypanosomiasis.Journal of medicinal chemistry · 2014Article
- High-throughput chemical screening for antivirulence developmental phenotypes in Trypanosoma brucei.Eukaryotic cell · 2014Article
- Article
- Regulators of Trypanosoma brucei cell cycle progression and differentiation identified using a kinome-wide RNAi screen.PLoS pathogens · 2014Article
- Distinct roles of a mitogen-activated protein kinase in cytokinesis between different life cycle forms of Trypanosoma brucei.Eukaryotic cell · 2014Article
- Hypothemycin, a fungal natural product, identifies therapeutic targets in Trypanosoma brucei [corrected].eLife · 2013Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
African trypanosomes undergo differentiation in order to adapt to the mammalian host and the tsetse fly vector. To characterize the role of a mitogen-activated protein (MAP) kinase homologue, TbMAPK5, in the differentiation of Trypanosoma brucei, we constructed a knockout in procyclic (insect) forms from a differentiation-competent (pleomorphic) stock. Two independent knockout clones proliferated normally in culture and were not essential for other life cycle stages in the fly. They were also able to infect immunosuppressed mice, but the peak parasitemia was 16-fold lower than that of the wild type. Differentiation of the proliferating long slender to the nonproliferating short stumpy bloodstream form is triggered by an autocrine factor, stumpy induction factor (SIF). The knockout differentiated prematurely in mice and in culture, suggestive of increased sensitivity to SIF. In contrast, a null mutant of a cell line refractory to SIF was able to proliferate normally. The differentiation phenotype was partially rescued by complementation with wild-type TbMAPK5 but exacerbated by introduction of a nonactivatable mutant form. Our results indicate a regulatory function for TbMAPK5 in the differentiation of bloodstream forms of T. brucei that might be exploitable as a target for chemotherapy against human sleeping sickness.
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