March 22, 2019
Division of Biology Seminar today
Matthew Wiebe, associate professor in the School of Veterinary and Biomedical Sciences at the University of Nebraska, Lincoln, will present "Genetic Conflict and Signaling Mimicry: Lessons from Poxvirus-Host Interaction" as part of the Division of Biology Seminar Series at 4 p.m. Friday, March 22, in 221 Ackert Hall.
Wiebe will discuss the Vaccinia virus and how it is the archetype member of the Poxviridae family. This virus encodes ~200 genes that contribute to viral propagation in the cytoplasm and coordinate restriction of the host antiviral response. Among these genes, the viral B1 kinase inhibits a highly conserved antiviral protein, allowing viral DNA replication to proceed in the cytoplasm. We have discovered that B1 performs this function by closely mimicking cellular signaling pathways, which normally guard cellular genomic integrity during mitosis. To further understand B1-driven signaling, Wiebe has also used experimental evolution of a B1 deletion virus to identify viral genes within shared signaling pathways.
This seminar will describe his success in isolating adapted viruses and the discovery of a genetic link between B1 and the related B12 gene. Thus, this study illustrates the utility of experimental evolution to discover novel conflicts between poxviral genes. Specifically, they elucidated an unexpected regulatory intersection between the B1 kinase and B12 pseudokinase that likely masked discovery of the repressive function of B12 during previous studies of this factor. As kinase-pseudokinase protein families are abundant in many forms of life, the genetic and functional relationship between B1 and B12 that will be discussed is likely of broad biological relevance.
If you would like to visit with Wiebe, contact Zhilong Yang at email@example.com.