Plant viral suppressors of post‐transcriptional silencing do not suppress transcriptional silencing

• Published in: The Plant journal : for cell and molecular biology Vol. 22; no. 1; pp. 51 - 59
• Main Authors: Marathe, Rajendra, Smith, Trenton H., Anandalakshmi, Radhamani, Bowman, Lewis H., Fagard, Mathilde, Mourrain, Philippe, Vaucheret, Hervé, Vance, Vicki B.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01-04-2000; Blackwell Science
• Subjects: Biological and medical sciences; Cucumber mosaic virus; Cucumovirus - genetics; Fundamental and applied biological sciences. Psychology; gene 271; Gene expression; Gene Silencing; Genes, Viral; H2 gene; Molecular and cellular biology; Molecular genetics; Nicotiana; Nii gene; Plant Viruses - genetics; Plants, Genetically Modified; Plants, Toxic; Potyvirus; Potyvirus - genetics; Suppression, Genetic; Transcription, Genetic; Plant pathogen; Transcription; Nicotiana tabacum; Posttranscriptional modification; Virus; Gene silencing; Regulation(control); Dicotyledones; Angiospermae; Suppressor; Spermatophyta; Potyvirus; Solanaceae; Experimental plant; Potyviridae
• ISSN: 0960-7412; 1365-313X
• DOI: 10.1046/j.1365-313x.2000.00710.x

Summary
Homology‐dependent gene silencing is a regulatory mechanism that limits RNA accumulation from affected loci either by suppression of transcription (transcriptional gene silencing, TGS) or by activation of a sequence‐specific RNA degradation process (post‐transcriptional gene silencing, PTGS). The P1/HC‐Pro sequence of plant potyviruses and the 2b gene of the cucumber mosaic virus have been shown to interfere with PTGS. The ability of these viral suppressors of PTGS to interfere with TGS was tested using the 271 locus which imposes TGS on transgenes under 35S or 19S promoters and PTGS on the endogenous nitrite reductase gene (Nii). Both P1/HC‐Pro and 2b reversed PTGS of Nii genes in 271‐containing tobacco plants, but failed to reverse TGS of 35S‐GUS transgenes in the same plant. P1/HC‐Pro expression from a transgene also failed to suppress either the initiation or maintenance of TGS imposed by the NOSpro‐silencing locus, H2. These results indicate that PTGS and TGS operate through unlinked pathways or that P1/HC‐Pro and 2b interfere at step(s) in PTGS that are downstream of any common components in the two pathways. The data suggest a simple assay to identify post‐transcriptionally silenced transgenic lines with the potential to be stably converted to high expressing lines.