Plant Antiviral Immunity Against Geminiviruses and Viral Counter-Defense for Survival.
TL;DR: This review summarizes the current knowledge concerning virus movement within and between cells, as well as the recent advances in the understanding of the biological roles of virus-encoded proteins in manipulating host-mediated responses and insect transmission.
Abstract: The family Geminiviridae includes plant-infecting viruses whose genomes are composed of one or two circular non-enveloped ssDNAs(+) of about 2.5-5.2 kb each in size. These insect-transmissible geminiviruses cause significant crop losses across continents and pose a serious threat to food security. Under the control of promoters generally located within the intergenic region, their genomes encode five to eight ORFs from overlapping viral transcripts. Most proteins encoded by geminiviruses perform multiple functions, such as suppressing defense responses, hijacking ubiquitin-proteasomal pathways, altering hormonal responses, manipulating cell cycle regulation, and exploiting protein-signaling cascades. Geminiviruses establish complex but coordinated interactions with several host elements to spread and facilitate successful infection cycles. Consequently, plants have evolved several multilayered defense strategies against geminivirus infection and distribution. Recent studies on the evasion of host-mediated resistance factors by various geminivirus proteins through novel mechanisms have provided new insights into the development of antiviral strategies against geminiviruses. This review summarizes the current knowledge concerning virus movement within and between cells, as well as the recent advances in our understanding of the biological roles of virus-encoded proteins in manipulating host-mediated responses and insect transmission. This review also highlights unexplored areas that may increase our understanding of the biology of geminiviruses and how to combat these important plant pathogens.
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TL;DR: These results suggest that nucleocytoplasmic shuttling of TLCYnV C4, enabled by phosphorylation by NbSKη, myristoylation, and interaction with exportin-α, is critical for its function as a pathogenicity factor.
64 citations
TL;DR: In this paper, the authors used tomato yellow leaf curl virus (TFLV) to demonstrate that some small ORFs are expressed during infection, and the encoded proteins display specific subcellular localizations.
Abstract: Geminiviruses are plant viruses with limited coding capacity. Geminivirus-encoded proteins are traditionally identified by applying a 10-kDa arbitrary threshold; however, it is increasingly clear that small proteins play relevant roles in biological systems, which calls for the reconsideration of this criterion. Here, we show that geminiviral genomes contain additional ORFs. Using tomato yellow leaf curl virus, we demonstrate that some of these small ORFs are expressed during the infection, and that the encoded proteins display specific subcellular localizations. We prove that the largest of these additional ORFs, which we name V3, is required for full viral infection, and that the V3 protein localizes in the Golgi apparatus and functions as an RNA silencing suppressor. These results imply that the repertoire of geminiviral proteins can be expanded, and that getting a comprehensive overview of the molecular plant-geminivirus interactions will require the detailed study of small ORFs so far neglected.
50 citations
Journal Article•
TL;DR: In this article, an automated bioinformatics workflow was developed and applied to identify core-genome differences between these two serovars with the aim to identify genome features associated with host specificity of S Pullorum.
36 citations
TL;DR: In this paper, the authors discuss the current knowledge of plant's antiviral responses exerted to geminivirus in the light of resistance mechanisms and the innate genetic factors contributing to the defence.
Abstract: Geminiviruses are circular, single-stranded viruses responsible for enormous crop loss worldwide. Rapid expansion of geminivirus diversity outweighs the continuous effort to control its spread. Geminiviruses channelize the host cell machinery in their favour by manipulating the gene expression, cell signalling, protein turnover, and metabolic reprogramming of plants. As a response to viral infection, plants have evolved to deploy various strategies to subvert the virus invasion and reinstate cellular homeostasis. Numerous reports exploring various aspects of plant-geminivirus interaction portray the subtlety and flexibility of the host–pathogen dynamics. To leverage this pool of knowledge towards raising antiviral resistance in host plants, a comprehensive account of plant’s defence response against geminiviruses is required. This review discusses the current knowledge of plant’s antiviral responses exerted to geminivirus in the light of resistance mechanisms and the innate genetic factors contributing to the defence. We have revisited the defence pathways involving transcriptional and post-transcriptional gene silencing, ubiquitin-proteasomal degradation pathway, protein kinase signalling cascades, autophagy, and hypersensitive responses. In addition, geminivirus-induced phytohormonal fluctuations, the subsequent alterations in primary and secondary metabolites, and their impact on pathogenesis along with the recent advancements of CRISPR-Cas9 technique in generating the geminivirus resistance in plants have been discussed. Considering the rapid development in the field of plant-virus interaction, this review provides a timely and comprehensive account of molecular nuances that define the course of geminivirus infection and can be exploited in generating virus-resistant plants to control global agricultural damage.
24 citations
TL;DR: This review focuses on the protein-protein network that converges on NSP with a high degree of centrality and forms an immune hub against begomoviruses and discusses the NSP virulence function as a suppressor of the recently described NSP-interacting kinase 1 (NIK1)-mediated antiviral immunity.
Abstract: 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.
23 citations
Cites background from "Plant Antiviral Immunity Against Ge..."
...Species of the Begomovirus genus can be either monopartite (with one single genomic component) or bipartite (two genomic components, referred to as DNA-A and DNA-B) (Zerbini et al., 2017; Kumar, 2019)....
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...The host range of begomovirus species depends on multiple molecular interactions involved in both co-opting the cellular machinery and evading the innate immune recognition (for reviews see Hanley-Bowdoin et al., 2013; Li et al., 2018; Kumar, 2019)....
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References
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TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Abstract: In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes.
For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure flux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy.
Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation, it is imperative to target by gene knockout or RNA interference more than one autophagy-related protein. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways implying that not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular assays, we hope to encourage technical innovation in the field.
5,187 citations
TL;DR: These studies uncover surprisingly pivotal roles of KIN10/11 in linking stress, sugar and developmental signals to globally regulate plant metabolism, energy balance, growth and survival.
Abstract: Photosynthetic plants are the principal solar energy converter sustaining life on Earth. Despite its fundamental importance, little is known about how plants sense and adapt to darkness in the daily light-dark cycle, or how they adapt to unpredictable environmental stresses that compromise photosynthesis and respiration and deplete energy supplies. Current models emphasize diverse stress perception and signalling mechanisms. Using a combination of cellular and systems screens, we show here that the evolutionarily conserved Arabidopsis thaliana protein kinases, KIN10 and KIN11 (also known as AKIN10/At3g01090 and AKIN11/At3g29160, respectively), control convergent reprogramming of transcription in response to seemingly unrelated darkness, sugar and stress conditions. Sensing and signalling deprivation of sugar and energy, KIN10 targets a remarkably broad array of genes that orchestrate transcription networks, promote catabolism and suppress anabolism. Specific bZIP transcription factors partially mediate primary KIN10 signalling. Transgenic KIN10 overexpression confers enhanced starvation tolerance and lifespan extension, and alters architecture and developmental transitions. Significantly, double kin10 kin11 deficiency abrogates the transcriptional switch in darkness and stress signalling, and impairs starch mobilization at night and growth. These studies uncover surprisingly pivotal roles of KIN10/11 in linking stress, sugar and developmental signals to globally regulate plant metabolism, energy balance, growth and survival. In contrast to the prevailing view that sucrose activates plant SnRK1s (Snf1-related protein kinases), our functional analyses of Arabidopsis KIN10/11 provide compelling evidence that SnRK1s are inactivated by sugars and share central roles with the orthologous yeast Snf1 and mammalian AMPK in energy signalling.
1,278 citations
TL;DR: Signaling pathways downstream of PRRs and their cross talk control immune responses in effective manners and can be negatively regulated by negative feedback mechanisms and also by anti-inflammatory factors such as TGFbeta, interleukin (IL)-10, and steroids.
Abstract: Pattern-recognition receptors (PRRs) initiate innate immunity through pathogen recognition. Serum PRRs opsonize pathogens for enhanced phagocytic clearance. Toll-like receptors (TLRs) initiate common NF-κB/AP-1 and distinct IRF3/7 pathways to coordinate innate immunity and to initiate adaptive immunity against diverse pathogens. Cytoplasmic caspase-recruiting domain (CARD) helicases, such as RIG-I/MDA5, mediate antiviral immunity by inducing the production of type I interferons via the adaptor IPS-1, whereas nucleotide-binding oligomerization domain (NOD)-like receptors mediate mainly antibacterial immunity by activating NF-κB or inflammasomes. Dectin-1 is important for antifungal immunity, promoting phagocytosis and activating NF-κB. Potentially harmful TLR signaling pathways can be negatively regulated by negative feedback mechanisms and also by anti-inflammatory factors such as TGFβ, interleukin (IL)-10, and steroids. Many combinations of TLR-TLR and TLR-NOD modulate inflammatory responses. TLR...
735 citations
"Plant Antiviral Immunity Against Ge..." refers background in this paper
...In animals, manipulation of innate immunity against viruses occurs via cross-talk between autophagy and several cellular components, such as pattern recognition receptors (PRRs) and macromolecular trafficking (Lee and Min, 2007)....
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TL;DR: Factors driving the emergence and establishment of whitefly-transmitted diseases include genetic changes in the virus through mutation and recombination, changes inThe vector populations coupled with polyphagy of the main vector, Bemisia tabaci, and long distance traffic of plant material or vector insects due to trade of vegetables and ornamental plants.
Abstract: Virus diseases that have emerged in the past two decades limit the production of important vegetable crops in tropical, subtropical, and temperate regions worldwide, and many of the causal viruses are transmitted by whiteflies (order Hemiptera, family Aleyrodidae). Most of these whitefly-transmitted viruses are begomoviruses (family Geminiviridae), although whiteflies are also vectors of criniviruses, ipomoviruses, torradoviruses, and some carlaviruses. Factors driving the emergence and establishment of whitefly-transmitted diseases include genetic changes in the virus through mutation and recombination, changes in the vector populations coupled with polyphagy of the main vector, Bemisia tabaci, and long distance traffic of plant material or vector insects due to trade of vegetables and ornamental plants. The role of humans in increasing the emergence of virus diseases is obvious, and the effect that climate change may have in the future is unclear.
732 citations
TL;DR: This Review describes the current knowledge of how geminiviruses interact with their plant hosts and the functional consequences of these interactions.
Abstract: The family Geminiviridae is one of the largest and most important families of plant viruses. The small, single-stranded DNA genomes of geminiviruses encode 5-7 proteins that redirect host machineries and processes to establish a productive infection. These interactions reprogramme plant cell cycle and transcriptional controls, inhibit cell death pathways, interfere with cell signalling and protein turnover, and suppress defence pathways. This Review describes our current knowledge of how geminiviruses interact with their plant hosts and the functional consequences of these interactions.
590 citations