RESUMO

Begomoviruses (Geminiviridae family) represent a severe constraint to agriculture worldwide. As ssDNA viruses that replicate in the nuclei of infected cells, the nascent viral DNA has to move to the cytoplasm and then to the adjacent cell to cause disease. The begomovirus nuclear shuttle protein (NSP) assists the intracellular transport of viral DNA from the nucleus to the cytoplasm and cooperates with the movement protein (MP) for the cell-to-cell translocation of viral DNA to uninfected cells. As a facilitator of intra- and intercellular transport of viral DNA, NSP is predicted to associate with host proteins from the nuclear export machinery, the intracytoplasmic active transport system, and the cell-to-cell transport complex. Furthermore, NSP functions as a virulence factor that suppresses antiviral immunity against begomoviruses. In this review, we focus on the protein-protein network that converges on NSP with a high degree of centrality and forms an immune hub against begomoviruses. We also describe the compatible host functions hijacked by NSP to promote the nucleocytoplasmic and intracytoplasmic movement of viral DNA. Finally, we discuss the NSP virulence function as a suppressor of the recently described NSP-interacting kinase 1 (NIK1)-mediated antiviral immunity. Understanding the NSP-host protein-protein interaction (PPI) network will probably pave the way for strategies to generate more durable resistance against begomoviruses.

RESUMO

The Geminiviridae family is one of the most successful and largest families of plant viruses that infect a large variety of important dicotyledonous and monocotyledonous crops and cause significant yield losses worldwide. This broad spectrum of host range is only possible because geminiviruses have evolved sophisticated strategies to overcome the arsenal of antiviral defenses in such diverse plant species. In addition, geminiviruses evolve rapidly through recombination and pseudo-recombination to naturally create a great diversity of virus species with divergent genome sequences giving the virus an advantage over the host recognition system. Therefore, it is not surprising that efficient molecular strategies to combat geminivirus infection under open field conditions have not been fully addressed. In this review, we present the anti-geminiviral arsenal of plant defenses, the evolved virulence strategies of geminiviruses to overcome these plant defenses and the most recent strategies that have been engineered for transgenic resistance. Although, the in vitro reactivation of suppressed natural defenses as well as the use of RNAi and CRISPR/Cas systems hold the potential for achieving broad-range resistance and/or immunity, potential drawbacks have been associated with each case.

Assuntos

RESUMO

Activation of antiviral innate immune responses depends on the recognition of viral components or viral effectors by host receptors. This virus recognition system can activate two layers of host defence, pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI). While ETI has long been recognized as an efficient plant defence against viruses, the concept of antiviral PTI has only recently been integrated into virus-host interaction models, such as the RNA silencing-based defences that are triggered by viral dsRNA PAMPs produced during infection. Emerging evidence in the literature has included the classical PTI in the antiviral innate immune arsenal of plant cells. Therefore, our understanding of PAMPs has expanded to include not only classical PAMPS, such as bacterial flagellin or fungal chitin, but also virus-derived nucleic acids that may also activate PAMP recognition receptors like the well-documented phenomenon observed for mammalian viruses. In this review, we discuss the notion that plant viruses can activate classical PTI, leading to both unique antiviral responses and conserved antipathogen responses. We also present evidence that virus-derived nucleic acid PAMPs may elicit the NUCLEAR SHUTTLE PROTEIN-INTERACTING KINASE 1 (NIK1)-mediated antiviral signalling pathway that transduces an antiviral signal to suppress global host translation.

Assuntos

RESUMO

Begomovirus-associated epidemics currently threaten tomato production worldwide due to the emergence of highly pathogenic virus species and the proliferation of a whitefly B biotype vector that is adapted to tomato. To generate an efficient defence against begomovirus, we modulated the activity of the immune defence receptor nuclear shuttle protein (NSP)-interacting kinase (NIK) in tomato plants; NIK is a virulence target of the begomovirus NSP during infection. Mutation of T474 within the kinase activation loop promoted the constitutive activation of NIK-mediated defences, resulting in the down-regulation of translation-related genes and the suppression of global translation. Consistent with these findings, transgenic lines harbouring an activating mutation (T474D) were tolerant to the tomato-infecting begomoviruses ToYSV and ToSRV. This phenotype was associated with reduced loading of coat protein viral mRNA in actively translating polysomes, lower infection efficiency and reduced accumulation of viral DNA in systemic leaves. Our results also add some relevant insights into the mechanism underlying the NIK-mediated defence. We observed that the mock-inoculated T474D-overexpressing lines showed a constitutively infected wild-type transcriptome, indicating that the activation of the NIK-mediated signalling pathway triggers a typical response to begomovirus infection. In addition, the gain-of-function mutant T474D could sustain an activated NIK-mediated antiviral response in the absence of the virus, further confirming that phosphorylation of Thr-474 is the crucial event that leads to the activation of the kinase.

Assuntos