Abstract
Viruses are dependent on host factors at all parts of the infection cycle, such as translation, genome replication, encapsidation, and cell-to-cell and systemic movement. RNA viruses replicate their genome in compartments associated with the endoplasmic reticulum, chloroplasts, and mitochondria or peroxisome membranes. In contrast, DNA viruses replicate in the nucleus. Viral infection causes changes in plant gene expression and in the subcellular localization of some host proteins. These changes may support or inhibit virus accumulation and spread. Here, we review host proteins that change their subcellular localization in the presence of a plant virus. The most frequent change is the movement of host cytoplasmic proteins into the sites of virus replication through interactions with viral proteins, and the protein contributes to essential viral processes. In contrast, only a small number of studies document changes in the subcellular localization of proteins with antiviral activity. Understanding the changes in the subcellular localization of host proteins during plant virus infection provides novel insights into the mechanisms of plant–virus interactions and may help the identification of targets for designing genetic resistance to plant viruses.
Highlights
Introduction and Katalin NemesThe most abundant plant viruses have a genome that is a positive single-strand RNA (Group IV) or a negative single-strand RNA (Group V)
We present an analysis of publications documenting changes in the subcellular localization of host proteins following viral infection
After profiling features of these proteins and viruses, several general patterns emerged: (1) 45 of the 55 combinations were identified using model hosts (Arabidopsis thaliana, Nicotiana benthamiana, or Saccharomyces cerevisiae, Figure 1A); (2) the majority (48) were identified using model positive-strand RNA viruses (Figure 1C), brome mosaic virus (BMV), tomato bushy stunt virus (TBSV), and turnip mosaic virus (TuMV) (Figure 1D); (3) in 46 of the 55 combinations, the host protein is beneficial to the virus; (4) host proteins with antiviral roles were less abundant (Figure 1B); and (5) the most frequent group (30 out of 55) was host proteins that moved from the cytoplasm to the sites of virus replication (Figure 2A and Table 2) through interactions with viral proteins (Table 2)
Summary
The most abundant plant viruses have a genome that is a positive single-strand RNA (Group IV) or a negative single-strand RNA (Group V). Viral nucleic acids and proteins execute their functions in cooperation with host proteins, RNAs, or other factors such as membranes or lipids [3,4] These components condition susceptibility, and their absence reduces virus accumulation or movement, and may turn a host into a nonhost. Viral infection induces changes in host gene expression [8,9] resulting in the upregulation of susceptibility genes [10] and activation or downregulation of antiviral defense responses [11,12], and may lead to up- or downregulation of genes that have no effect on the virus [8,9]. Antiviral defense is mediated by host factors that target viral proteins or nucleic acids and antagonize key parts of virus replication and/or movement, reducing virus accumulation or limiting the spread of infection within the plant [7,15]. The profiles advance our understanding of the mechanisms that govern plant–virus interactions and establish the basis for the identification of novel host factors with antiviral activity or that condition virus susceptibility and that can be targeted to generate virus-resistant plants by genetic engineering
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