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Updated: Apr 5, 2026

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
KU80, a key factor for non-homologous end-joining, retards geminivirus multiplication
Kathrin S Richter1, Holger Jeske1
1Institute of Biomaterials and Biomolecular Systems, Department of Molecular Biology and Plant Virology, University of Stuttgart, Pfaffenwaldring 57, D-70550 Stuttgart, Germany.
Abstract:
KU80 is well-known as a key component of the non-homologous end-joining pathway used to repair DNA double-strand breaks. In addition, the KU80-containing DNA-dependent protein kinase complex in mammals can act as a cytoplasmic sensor for viral DNA to activate innate immune response. We have now, to our knowledge for the first time, demonstrated that the speed of a systemic infection with a plant DNA geminivirus in Arabidopsis thaliana is KU80-dependent. The early emergence of Euphorbia yellow mosaic virus DNA was significantly increased in ku80 knockout mutants compared with wild-type sibling controls. The possible impact of KU80 on geminivirus multiplication by generating non-productive viral DNAs or its role as a pattern-recognition receptor against DNA virus infection is discussed.
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