Control of Nuclear and Nucleolar Localization of Nuclear Inclusion Protein a of Picorna-Like<i>Potato virus A</i>in<i>Nicotiana</i>Species

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

doi:10.1105/tpc.108.064147

Cited by 138 publications

(162 citation statements)

References 91 publications

(132 reference statements)

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“…It is possible that NIa-Pro also cleaves a plant protein that possesses the NIa-Pro cleavage substrate. Yet NIa-Pro also has other functions, including nonspecific DNAse activity (Anindya and Savithri, 2004;Rajamäki and Valkonen, 2009), and may possess additional unknown functions that are critical to aphidvirus-plant interactions.…”

Section: Discussionmentioning

confidence: 99%

Disruption of Ethylene Responses by Turnip mosaic virus Mediates Suppression of Plant Defense against the Green Peach Aphid Vector

Casteel

Alwis²,

Bak³

et al. 2015

Plant Physiol.

138

129

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Plants employ diverse responses mediated by phytohormones to defend themselves against pathogens and herbivores. Adapted pathogens and herbivores often manipulate these responses to their benefit. Previously, we demonstrated that Turnip mosaic virus (TuMV) infection suppresses callose deposition, an important plant defense induced in response to feeding by its aphid vector, the green peach aphid (Myzus persicae), and increases aphid fecundity compared with uninfected control plants. Further, we determined that production of a single TuMV protein, Nuclear Inclusion a-Protease (NIa-Pro) domain, was responsible for changes in host plant physiology and increased green peach aphid reproduction. To characterize the underlying molecular mechanisms of this phenomenon, we examined the role of three phytohormone signaling pathways, jasmonic acid, salicylic acid, and ethylene (ET), in TuMV-infected Arabidopsis (Arabidopsis thaliana), with or without aphid herbivory. Experiments with Arabidopsis mutants ethylene insensitive2 and ethylene response1, and chemical inhibitors of ET synthesis and perception (aminoethoxyvinyl-glycine and 1-methylcyclopropene, respectively), show that the ET signaling pathway is required for TuMV-mediated suppression of Arabidopsis resistance to the green peach aphid. Additionally, transgenic expression of NIa-Pro in Arabidopsis alters ET responses and suppresses aphidinduced callose formation in an ET-dependent manner. Thus, disruption of ET responses in plants is an additional function of NIaPro, a highly conserved potyvirus protein. Virus-induced changes in ET responses may mediate vector-plant interactions more broadly and thus represent a conserved mechanism for increasing transmission by insect vectors across generations.

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Section: Discussionmentioning

confidence: 99%

Disruption of Ethylene Responses by Turnip mosaic virus Mediates Suppression of Plant Defense against the Green Peach Aphid Vector

Casteel

Alwis²,

Bak³

et al. 2015

Plant Physiol.

138

129

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“…More recently, another short ORF, termed PISPO (pretty interesting sweet potato potyvirus ORF), also resulting from transcriptional slippage, was found to be embedded in the P1 coding regions of two sweet potato potyviruses (26,30,31). Among the 11 common potyvirus proteins, HC-Pro and VPg have been shown to be VSRs (32)(33)(34). The molecular mechanisms underlying the functional role of HC-Pro as a VSR have been relatively well understood (35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46).…”

mentioning

confidence: 99%

The Potyvirus Silencing Suppressor Protein VPg Mediates Degradation of SGS3 via Ubiquitination and Autophagy Pathways

Cheng

Wang

2017

J Virol

139

123

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RNA silencing is an innate antiviral immunity response of plants and animals. To counteract this host immune response, viruses have evolved an effective strategy to protect themselves by the expression of viral suppressors of RNA silencing (VSRs). Most potyviruses encode two VSRs, helper component-proteinase (HCPro) and viral genome-linked protein (VPg). The molecular biology of the former has been well characterized, whereas how VPg exerts its function in the suppression of RNA silencing is yet to be understood. In this study, we show that infection by Turnip mosaic virus (TuMV) causes reduced levels of suppressor of gene silencing 3 (SGS3), a key component of the RNA silencing pathway that functions in doublestranded RNA synthesis for virus-derived small interfering RNA (vsiRNA) production. We also demonstrate that among 11 TuMV-encoded viral proteins, VPg is the only one that interacts with SGS3. We furthermore present evidence that the expression of VPg alone, independent of viral infection, is sufficient to induce the degradation of SGS3 and its intimate partner RNA-dependent RNA polymerase 6 (RDR6). Moreover, we discover that the VPg-mediated degradation of SGS3 occurs via both the 20S ubiquitin-proteasome and autophagy pathways. Taken together, our data suggest a role for VPg-mediated degradation of SGS3 in suppression of silencing by VPg.IMPORTANCE Potyviruses represent the largest group of known plant viruses and cause significant losses of many agriculturally important crops in the world. In order to establish infection, potyviruses must overcome the host antiviral silencing response. A viral protein called VPg has been shown to play a role in this process, but how it works is unclear. In this paper, we found that the VPg protein of Turnip mosaic virus (TuMV), which is a potyvirus, interacts with a host protein named SGS3, a key protein in the RNA silencing pathway. Moreover, this interaction leads to the degradation of SGS3 and its interacting and functional partner RDR6, which is another essential component of the RNA silencing pathway. We also identified the cellular pathways that are recruited for the VPg-mediated degradation of SGS3. Therefore, this work reveals a possible mechanism by which VPg sabotages host antiviral RNA silencing to promote virus infection. KEYWORDS RDR6, RNA silencing, SGS3, VPg, VSR, autophagy, potyvirus, ubiquitination T o establish systemic infection, an invading virus must remodel and recruit host elements and overcome resistance responses through complex molecular virushost interactions (1-3). One such essential antiviral response is RNA silencing (4-6), a cellular mechanism conserved from lower eukaryotes to mammals to regulate endogenous gene expression at the transcriptional and posttranscriptional levels (7, 8). To activate antiviral RNA silencing, the viral double-stranded RNAs (dsRNAs), which may

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“…Amino acids 38 to 44 of PVA VPg are responsible for nucleotide triphosphate (NTP) binding, and their deletion impairs uridylylation of VPg (35). Furthermore, this region contains the second part of the bipartite nuclear localization signal (NLS) of PVA VPg (amino acids 41 to 50) (38). Replication of positive-sense RNA viruses takes place in the cytoplasm in compartments formed from hostderived membranes (7,28).…”

mentioning

confidence: 99%

Structural Flexibility Allows the Functional Diversity of Potyvirus Genome-Linked Protein VPg

Rantalainen

Eskelin

Tompa

et al. 2011

J Virol

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Control of Nuclear and Nucleolar Localization of Nuclear Inclusion Protein a of Picorna-LikePotato virus AinNicotianaSpecies

Cited by 138 publications

References 91 publications

Disruption of Ethylene Responses by Turnip mosaic virus Mediates Suppression of Plant Defense against the Green Peach Aphid Vector

Disruption of Ethylene Responses by Turnip mosaic virus Mediates Suppression of Plant Defense against the Green Peach Aphid Vector

The Potyvirus Silencing Suppressor Protein VPg Mediates Degradation of SGS3 via Ubiquitination and Autophagy Pathways

Structural Flexibility Allows the Functional Diversity of Potyvirus Genome-Linked Protein VPg

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