The Interaction between geminivirus pathogenicity proteins and adenosine kinase leads to increased expression of primary cytokinin-responsive genes |
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Authors: | Surendranath Baliji Garry Sunter |
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Affiliation: | a Department of Biology, The University of Texas at San Antonio, San Antonio, TX 78249, USA b Department of Microbiology and Immunology, Loyola University Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA c Tumor Virology Program, Greheey Children's Cancer Research Institute, The University of Texas Health Sciences Center, San Antonio, San Antonio, TX 78229, USA |
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Abstract: | Pathogenicity proteins (AL2/C2) of begomo- and curtoviruses suppress silencing through inhibition of the methyl cycle, as a consequence of inhibiting adenosine kinase (ADK). ADK phosphorylates cytokinin nucleosides, helping maintain a pool of bioactive cytokinins through interconversion of free-bases, nucleosides and nucleotides. We provide evidence that inhibiting ADK affects expression of primary cytokinin-responsive genes. Specifically, we demonstrate increased activity of a primary cytokinin-responsive promoter in adk mutant Arabidopsis plants, and in response to silencing ADK expression or inhibiting ADK activity in transient assays. Similar changes in expression are observed in geminivirus infected tissue and when AL2/C2 are over-expressed. Increased cytokinin-responsive promoter activity may therefore be a consequence of an ADK/AL2/C2 interaction. Application of exogenous cytokinin increases susceptibility to geminivirus infection, characterized by a reduced mean latent period and enhanced viral replication. Thus, ADK appears to be a high value target of geminiviruses that includes increasing expression of primary cytokinin-responsive genes. |
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Keywords: | Geminivirus Cytokinins Cell cycle ADK AL2 C2 Silencing |
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