Improved silencing suppression and enhanced heterologous protein expression are achieved using an engineered viral helper component proteinase

Haikonen, Tuuli; Rajamäki, Minna-Liisa; Valkonen, Jari P. T.

doi:10.1016/j.jviromet.2013.07.054

Cited by 6 publications

(2 citation statements)

References 49 publications

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“…PTGS is frequently activated during transgenesis and manifests with lowered efficiency of transgene expression. Therefore, the appearance of a strong RSS can elevate the production efficiency of the recombinant protein (Gao et al 2013 ; Garabagi et al 2012 ; Haikonen et al 2013 ; reviewed by Saunders and Lomonossoff 2013 ; Sun et al 2011 ). However, in transgenic plants stably expressing RSS, unfavorable harmful developmental effects were observed.…”

Section: Discussionmentioning

confidence: 99%

Suppress to Survive—Implication of Plant Viruses in PTGS

Wieczorek

Obrępalska‐Stęplowska

2014

Plant Mol Biol Rep

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In higher plants, evolutionarily conserved processes playing an essential role during gene expression rely on small noncoding RNA molecules (sRNA). Within a wide range of sRNA-dependent cellular events, there is posttranscriptional gene silencing, the process that is activated in response to the presence of double-stranded RNAs (dsRNAs) in planta. The sequence-specific mechanism of silencing is based on RNase-mediated trimming of dsRNAs into translationally inactive short molecules. Viruses invading and replicating in host are also a source of dsRNAs and are recognized as such by cellular posttranscriptional silencing machinery leading to degradation of the pathogenic RNA. However, viruses are not totally defenseless. In parallel with evolving plant defense strategies, viruses have managed a wide range of multifunctional proteins that efficiently impede the posttranscriptional gene silencing. These viral counteracting factors are known as suppressors of RNA silencing. The aim of this review is to summarize the role and the mode of action of several functionally characterized RNA silencing suppressors encoded by RNA viruses directly involved in plant–pathogen interactions. Additionally, we point out that the widely diverse functions, structures, and modes of action of viral suppressors can be performed by different proteins, even in related viruses. All those adaptations have been evolved to achieve the same goal: to maximize the rate of viral genetic material replication by interrupting the evolutionary conserved plant defense mechanism of posttranscriptional gene silencing.

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Section: Discussionmentioning

confidence: 99%

Suppress to Survive—Implication of Plant Viruses in PTGS

Wieczorek

Obrępalska‐Stęplowska

2014

Plant Mol Biol Rep

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“…A viral suppressor is a key regulator for counteracting the RNA-silencing defense in plants [13–15]. Because of silencing suppression, foreign proteins in viral vector-infected plants are expressed to a higher degree than in transgenic plants [16–18]. In addition, the viral suppressor interferes microRNA (miRNA) biogenesis, resulting in severe symptoms that affect the normal growth status of host plants [19, 20].…”

Section: Introductionmentioning

confidence: 99%

Development of a Mild Viral Expression System for Gain-Of-Function Study of Phytoplasma Effector In Planta

Huang

Lin

et al. 2015

PLoS ONE

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PHYL1 and SAP54 are orthologs of pathogenic effectors of Aster yellow witches’-broom (AYWB) phytoplasma and Peanut witches’-broom (PnWB) phytoplasma, respectively. These effectors cause virescence and phyllody symptoms (hereafter leafy flower) in phytoplasma-infected plants. T0 lines of transgenic Arabidopsis expressing the PHYL1 or SAP54 genes (PHYL1 or SAP54 plants) show a leafy flower phenotype and result in seedless, suggesting that PHYL1 and SAP54 interfere with reproduction stage that restrict gain-of-function studies in the next generation of transgenic plants. Turnip mosaic virus (TuMV) mild strain (TuGK) has an Arg182Lys mutation in the helper-component proteinase (HC-ProR182K) that blocks suppression of the miRNA pathway and prevents symptom development in TuGK-infected plants. We exploited TuGK as a viral vector for gain-of-function studies of PHYL1 and SAP54 in Arabidopsis plants. TuGK-PHYL1- and TuGK-SAP54-infected Arabidopsis plants produced identical leafy flower phenotypes and similar gene expression profiles as PHYL1 and SAP54 plants. In addition, the leafy flower formation rate was enhanced in TuGK-PHYL1- or TuGK-SAP54-infected Arabidopsis plants that compared with the T0 lines of PHYL1 plants. These results provide more evidence and novel directions for further studying the mechanism of PHYL1/SAP54-mediated leafy flower development. In addition, the TuGK vector is a good alternative in transgenic plant approaches for rapid gene expression in gain-of-function studies.

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