Poster
Delphine Maya Pott
Department of Plant Biochemistry, Centre for Plant Molecular Biology (ZMBP), Eberhard Karls University
Tuebingen, Baden-Wurttemberg, Germany
Liping Wang
Max Planck Institute for Biology Tübingen
Tübingen, Tübingen, GERMANY
Chaonan Shi
PhD
Department of Plant Biochemistry, Centre for Plant Molecular Biology (ZMBP), Eberhard Karls University
Tübingen, Baden-Wurttemberg, Germany
Laura Medina-Puche
Department of Plant Biochemistry, Centre for Plant Molecular Biology (ZMBP), Eberhard Karls University
Tubingen, Baden-Wurttemberg, Germany
Gemma Sans-Coll
IHSM-University of Malaga-CSIC
Malaga, Andalucia, Spain
Björn Krenz
Leibniz Institute DSMZ
Braunschweig, Niedersachsen, Germany
Catharina Merchante
IHSM-University of Malaga-CSIC
Malaga, Andalucia, Spain
Rosa Lozano-Durán
University of Tübingen
Tübingen, GERMANY
Despite very limited coding capacity, viruses efficiently replicate and spread using intricate strategies, which are not yet fully understood. Geminiviruses are emergent plant pathogens with diminutive single-stranded DNA genomes; they replicate in the nucleus through the action of the viral replication-associated protein (Rep), which shows the highest conservation among geminiviruses and other related viruses. Rep recruits the host DNA replication machinery to the viral DNA; it also represses the promoter of its own gene to control the infection cycle. To mediate both functions, Rep binds the same site in the viral genome; however, how both activities are regulated remains elusive. We found that tomato yellow leaf curl virus (TYLCV) subverts the host splicing machinery to generate shorter Rep spliced variants. These novel isoforms are unable to initiate replication due to the loss of the central oligomerization domain, essential for this function. However, they strongly repress Rep promoter, while mutants impaired in splicing fail to do so. Decreased Rep splicing results in inefficient viral gene regulation and reduced infectivity. We outline a novel viral strategy to produce functionally-specialized isoforms, with Rep spliced variants as the long-sought mechanism explaining Rep dual role as master regulator of replication and gene expression. This approach may be shared by viruses infecting all domains of life, as similar splicing events occur in their Rep transcripts.