scholarly journals Expression analysis of host defense responses against the 8K (KDa) cysteine-rich viral silencing suppressor protein in Nicotiana benthamiana

Plant Omics ◽  
2018 ◽  
Vol 11 (02) ◽  
pp. 113-119
Author(s):  
Aminallah Tahmasebi ◽  
◽  
Alireza Afsharifar ◽  
Ahmad Heydari ◽  
Mohammad Mehrabadi ◽  
...  
2018 ◽  
Vol 31 (1) ◽  
pp. 86-100 ◽  
Author(s):  
Sylvain Poque ◽  
Hui-Wen Wu ◽  
Chung-Hao Huang ◽  
Hao-Wen Cheng ◽  
Wen-Chi Hu ◽  
...  

The viral infection process is a battle between host defense response and pathogen antagonizing action. Several studies have established a tight link between the viral RNA silencing suppressor (RSS) and the repression of salicylic acid (SA)-mediated defense responses, nonetheless host factors directly linking an RSS and the SA pathway remains unidentified. From yeast two-hybrid analysis, we identified an interaction between the potyviral RSS helper-component proteinase (HCPro) and SA–binding protein SABP3. Co-localization and bimolecular fluorescence complementation analyses validated the direct in vivo interaction between Turnip mosaic virus (TuMV) HCPro and the Arabidopsis homologue of SABP3, AtCA1. Additionally, transient expression of TuMV HCPro demonstrated its ability to act as a negative regulator of AtCA1. When the plants of the AtCA1 knockout mutant line were inoculated with TuMV, our results indicated that AtCA1 is essential to restrict viral spreading and accumulation, induce SA accumulation, and trigger the SA pathway. Unexpectedly, the AtCA1 overexpression line also displayed a similar phenotype, suggesting that the constitutive expression of AtCA1 antagonizes the SA pathway. Taken together, our results depict AtCA1 as an essential regulator of SA defense responses. Moreover, the interaction of potyviral HCPro with this regulator compromises the SA pathway to weaken host defense responses and facilitate viral infection.


Viruses ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 195
Author(s):  
Song Guo ◽  
Sek-Man Wong

A carboxylesterase (CXE) or carboxylic-ester hydrolase is an enzyme that catalyzes carboxylic ester and water into alcohol and carboxylate. In plants, CXEs have been implicated in defense, development, and secondary metabolism. We discovered a new CXE gene in Nicotiana benthamiana that is related to virus resistance. The transcriptional level of NbCXE expression was significantly increased after Tobacco mosaic virus (TMV) infection. Transient over-expression of NbCXE inhibited TMV accumulation in N. benthamiana plants. Conversely, when the NbCXE gene was silenced with a Tobacco rattle virus (TRV)-based gene silencing system, TMV RNA accumulation was increased in NbCXE-silenced plants after infection. NbCXE protein was shown to interact with TMV coat protein (CP) in vitro. Additionally, the expressions of host defense-related genes were increased in transient NbCXE-overexpressed plants but decreased in NbCXE silenced N. benthamiana plants. In summary, our study showed that NbCXE is a novel resistance-related gene involved in host defense responses against TMV infection.


PLoS ONE ◽  
2012 ◽  
Vol 7 (12) ◽  
pp. e52717 ◽  
Author(s):  
Fatima Naim ◽  
Kenlee Nakasugi ◽  
Ross N. Crowhurst ◽  
Elena Hilario ◽  
Alexander B. Zwart ◽  
...  

2007 ◽  
Vol 81 (22) ◽  
pp. 12285-12297 ◽  
Author(s):  
Juan Jovel ◽  
Melanie Walker ◽  
Hélène Sanfaçon

ABSTRACT Recovery of plants from virus-induced symptoms is often described as a consequence of RNA silencing, an antiviral defense mechanism. For example, recovery of Nicotiana clevelandii from a nepovirus (tomato black ring virus) is associated with a decreased viral RNA concentration and sequence-specific resistance to further virus infection. In this study, we have characterized the interaction of another nepovirus, tomato ringspot virus (ToRSV), with host defense responses during symptom induction and subsequent recovery. Early in infection, ToRSV induced a necrotic phenotype in Nicotiana benthamiana that showed characteristics typical of a hypersensitive response. RNA silencing was also activated during ToRSV infection, as evidenced by the presence of ToRSV-derived small interfering RNAs (siRNAs) that could direct degradation of ToRSV sequences introduced into sensor constructs. Surprisingly, disappearance of symptoms was not accompanied by a commensurate reduction in viral RNA levels. The stability of ToRSV RNA after recovery was also observed in N. clevelandii and Cucumis sativus and in N. benthamiana plants carrying a functional RNA-dependent RNA polymerase 1 ortholog from Medicago truncatula. In experiments with a reporter transgene (green fluorescent protein), ToRSV did not suppress the initiation or maintenance of transgene silencing, although the movement of the silencing signal was partially hindered. Our results demonstrate that although RNA silencing is active during recovery, reduction of virus titer is not required for the initiation of this phenotype. This scenario adds an unforeseen layer of complexity to the interaction of nepoviruses with the host RNA silencing machinery. The possibility that viral proteins, viral RNAs, and/or virus-derived siRNAs inactivate host defense responses is discussed.


2021 ◽  
Vol 22 (8) ◽  
pp. 4224
Author(s):  
Urban Kunej ◽  
Jernej Jakše ◽  
Sebastjan Radišek ◽  
Nataša Štajner

RNA interference is an evolutionary conserved mechanism by which organisms regulate the expression of genes in a sequence-specific manner to modulate defense responses against various abiotic or biotic stresses. Hops are grown for their use in brewing and, in recent years, for the pharmaceutical industry. Hop production is threatened by many phytopathogens, of which Verticillium, the causal agent of Verticillium wilt, is a major contributor to yield losses. In the present study, we performed identification, characterization, phylogenetic, and expression analyses of three Argonaute, two Dicer-like, and two RNA-dependent RNA polymerase genes in the susceptible hop cultivar Celeia and the resistant cultivar Wye Target after infection with Verticillium nonalfalfae. Phylogeny results showed clustering of hop RNAi proteins with their orthologues from the closely related species Cannabis sativa, Morus notabilis and Ziziphus jujuba which form a common cluster with species of the Rosaceae family. Expression analysis revealed downregulation of argonaute 2 in both cultivars on the third day post-inoculation, which may result in reduced AGO2-siRNA-mediated posttranscriptional gene silencing. Both cultivars may also repress ta-siRNA biogenesis at different dpi, as we observed downregulation of argonaute 7 in the susceptible cultivar on day 1 and downregulation of RDR6 in the resistant cultivar on day 3 after inoculation.


2017 ◽  
Vol 100 ◽  
pp. 22-32 ◽  
Author(s):  
Diana Tamayo ◽  
José F. Muñoz ◽  
Agostinho J. Almeida ◽  
Juan D. Puerta ◽  
Ángela Restrepo ◽  
...  

2009 ◽  
Vol 9 (1) ◽  
pp. 96 ◽  
Author(s):  
Raffaele Lombardi ◽  
Patrizia Circelli ◽  
Maria Villani ◽  
Giampaolo Buriani ◽  
Luca Nardi ◽  
...  

2001 ◽  
Vol 280 (5) ◽  
pp. R1434-R1439 ◽  
Author(s):  
Lisa E. Goehler ◽  
Ron P. A. Gaykema ◽  
Michael K. Hansen ◽  
Jayme L. Kleiner ◽  
Steven F. Maier ◽  
...  

The paraventricular nucleus of the hypothalamus (PVH) occupies a pivotal point within the network of brain nuclei coordinating critical host-defense responses. In mice, T cell-dependent immune stimuli, including the bacterial superantigen staphylococcal enterotoxin B (SEB), can activate the PVH. To determine whether T cell-dependent immune stimuli activate the PVH in rats, we assessed plasma corticosterone (Cort) levels, fever responses, and c-Fos expression in the PVH in animals treated with intraperitoneal injections of SEB. In animals with previously implanted abdominal thermisters, intraperitoneal injection of 1 mg/kg SEB resulted in a significant rise in body temperature, with a latency of 3.5–4 h. In separate animals, intraperitoneal injection of 1 mg/kg SEB resulted in a significant elevation of plasma Cort and induced c-Fos expression in parvocellular neurons within the PVH. These results support the idea that T cell-dependent immune stimuli activate brain pathways mediating host-defense responses such as fever and neuroendocrine changes.


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