Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 104, Issue 29, Pages 12157-12162Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0705114104
Keywords
coat protein-mediated resistance; biomolecular fluorescence complementation; coat protein; movement protein
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Funding
- NIAID NIH HHS [R01 AI027161] Funding Source: Medline
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Infections by plant virus generally cause disease symptoms by interfering with cellular processes. Here we demonstrated that infection of Nicotiana tabacum (NA) by plant viruses representative of the Tobamoviridae, Potyviridae, and Potexviridae families altered accumulation of certain microRNAs (miRNAs). A correlation was observed between symptom severity and alteration in levels of miRNAs 156, 160, 164,166, 169, and 171 that is independent of viral posttranscriptional gene silencing suppressor activity. Hybrid transgenic plants that produced tobacco mosaic virus (TMV) movement protein (MIP) plus coat protein (Cp)(T42W) (a variant of CP) exhibited disease-like phenotypes, including abnormal plant development. Grafting studies with a plant line in which both transgenes are silenced confirmed that the disease-like phenotypes are due to the coexpression of CIP and MIP. In hybrid MpxCp(T42W) plants and TMV-infected plants, miRNAs 156,164,165, and 167 accumulated to higher levels compared with nontransgenic and noninfected tissues. Bimolecular fluorescence complementation assays revealed that MP interacts with CPT42W in vivo and leads to the hypothesis that complexes formed between MP and CP caused increases in miRNAs that result in disease symptoms. This work presents evidence that virus infection and viral proteins influence miRNA balance without affecting posttranscriptional gene silencing and contributes to the hypothesis that viruses exploit miRNA pathways during pathogenesis.
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