Linked Life Data

12586064

Source:http://linkedlifedata.com/resource/pubmed/id/12586064

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pubmed-article:12586064pubmed:abstractTextThe molecular basis for virus-induced disease in plants has been a long-standing mystery. Infection of Arabidopsis by Turnip mosaic virus (TuMV) induces a number of developmental defects in vegetative and reproductive organs. We found that these defects, many of which resemble those in miRNA-deficient dicer-like1 (dcl1) mutants, were due to the TuMV-encoded RNA-silencing suppressor, P1/HC-Pro. Suppression of RNA silencing is a counterdefensive mechanism that enables systemic infection by TuMV. The suppressor interfered with the activity of miR171 (also known as miRNA39), which directs cleavage of several mRNAs coding for Scarecrow-like transcription factors, by inhibiting miR171-guided nucleolytic function. Out of ten other mRNAs that were validated as miRNA-guided cleavage targets, eight accumulated to elevated levels in the presence of P1/HC-Pro. The basis for TuMV- and other virus-induced disease in plants may be explained, at least partly, by interference with miRNA-controlled developmental pathways that share components with the antiviral RNA-silencing pathway.lld:pubmed
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pubmed-article:12586064pubmed:articleTitleP1/HC-Pro, a viral suppressor of RNA silencing, interferes with Arabidopsis development and miRNA unction.lld:pubmed
pubmed-article:12586064pubmed:affiliationCenter for Gene Research and Biotechnology and Department of Botany and Plant Pathology, Oregon State University, Corvallis, OR 97331, USA.lld:pubmed
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pubmed-article:12586064pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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