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The Role of TAK1 in Yop J-induced Cell Death

Undergraduate #99
Discipline: Biological Sciences
Subcategory: Microbiology/Immunology/Virology

Alexandria Brooks - Alabama State University
Co-Author(s): Kristian Starheim and Egil Lien, University of Massachusetts Medical School, Worcester, MA



Yersinia Pestis (Yp) is a Gram-negative bacterium that is the causative agent of plague. This bacterium’s ability to evade the host’s innate immune system gives it a high virulence. Yp secretes multiple proteins, Yops, into the host immune cells. YopJ causes cell death in a RIPK1-dependent manner. RIPK1 activates a system of innate immune response pathways such as the proinflammatory NF-B pathway, Caspase-8 dependent apoptosis, IL-1b release and RIP3 dependent necroptosis. An important proinflammatory kinase downstream of RIPK1 is TAK1. It leads to activation of NF-κB and AP-1-dependent transcription of proinflammatory genes. We hypothesized that TAK1 can partake in a Yp-induced switch from NF-B activation to cell death in concert with other factors in the RIPK1/NF-B/ MAPK pathway. We show that ∆YopJ infection combined with TAK1-inhibition phenocopies YopJ-induced cell death in macrophages, indicating that TAK1 is a central factor in YopJinduced cell death and immune regulation.

Funder Acknowledgement(s): NIH

Faculty Advisor: Egil Lien,

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This material is based upon work supported by the National Science Foundation (NSF) under Grant No. DUE-1930047. Any opinions, findings, interpretations, conclusions or recommendations expressed in this material are those of its authors and do not represent the views of the AAAS Board of Directors, the Council of AAAS, AAAS’ membership or the National Science Foundation.

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