Theileria parasites subvert E2F signaling to stimulate leukocyte proliferation

Tretina, K. and Haidar, M. and Madsen-Bouterse, S. A. and Sakura, T. and Mfarrej, S. and Fry, L. and Chaussepied, M. and Pain, A. and Knowles, D. P. and Nene, V. M. and Ginsberger, D. and Daubenberger, C. and Bishop, R. P. and Langsley, G. and Silva , J.C.. (2020) Theileria parasites subvert E2F signaling to stimulate leukocyte proliferation. Scientific reports, 10. p. 3982.

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Intracellular pathogens have evolved intricate mechanisms to subvert host cell signaling pathways and ensure their own propagation. A lineage of the protozoan parasite genus Theileria infects bovine leukocytes and induces their uncontrolled proliferation causing a leukemia-like disease. Given the importance of E2F transcription factors in mammalian cell cycle regulation, we investigated the role of E2F signaling in Theileria-induced host cell proliferation. Using comparative genomics and surface plasmon resonance, we identified parasite-derived peptides that have the sequence-specific ability to increase E2F signaling by binding E2F negative regulator Retinoblastoma-1 (RB). Using these peptides as a tool to probe host E2F signaling, we show that the disruption of RB complexes ex vivo leads to activation of E2F-driven transcription and increased leukocyte proliferation in an infection-dependent manner. This result is consistent with existing models and, together, they support a critical role of E2F signaling for Theileria-induced host cell proliferation, and its potential direct manipulation by one or more parasite proteins.
Faculties and Departments:09 Associated Institutions > Swiss Tropical and Public Health Institute (Swiss TPH) > Department of Medical Parasitology and Infection Biology (MPI) > Clinical Immunology (Daubenberger)
UniBasel Contributors:Daubenberger, Claudia
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:British Antarctic Survey
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:11 Mar 2020 08:51
Deposited On:11 Mar 2020 08:51

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