Abstract
In the pathogen infection and host defence equilibrium, plant viruses have evolved to efficiently replicate their genomes, to resist the attack from host defence responses and to avoid causing severe negative effect on growth and metabolism of the hosts. In this study, we generated chimeric tobacco mosaic virus (TMV) variants, in which the coat protein (CP) sequences were substituted with that of cucumber green mottle mosaic virus (CGMMV) or pepper mild mottle virus (PMMoV) to address the role of these in virus infection and host symptomology. The results showed that the chimeric viruses (TMV-CGCP or TMV-PMCP) induce stunting and necrotic symptoms in tobacco plants. We analyzed the transcriptomic changes in tobacco plants after infection of TMV and its chimeras using a high-throughput RNA sequencing approach and found that infection of the chimeric TMV induced significant up-regulation of host defence responsive genes together with salicylic (SA) or abscisic acid (ABA) responsive genes, but down-regulation of auxin (Aux) responsive genes. We further confirmed the increase in the levels of SA and ABA, together with the reduced levels of Aux after infection of chimeric TMV in tobacco plants. These data suggest novel roles of tobamovirus CP in induction of host symptoms and defence responses.
Highlights
Plant viruses are obligate intracellular parasites and rely on the host machinery for the establishment of their infection cycle (McLeish et al, 2018)
A. tumefaciens GV3101 containing pCB-tobacco mosaic virus (TMV), pCB-TMV-CGCP or pCB-TMVPMCP were infiltrated into N. benthamiana leaves and visible shriveled symptoms appeared on the upper non-inoculated leaves at 5 dpi
The results showed that TMV together with the chimeric viruses can cause chlorosis and mosaic symptoms on the upper un-inoculated leaves of N. tabacum at 12 dpi (Figure 1C)
Summary
Plant viruses are obligate intracellular parasites and rely on the host machinery for the establishment of their infection cycle (McLeish et al, 2018). Virus-host interaction induces significant molecular alterations in the host plant, which leads to the display of disease symptoms (Lu et al, 2012). Plants usually develop symptoms such as mosaic, stunting, chlorosis or necrosis after virus infection, which may significantly reduce the quality of crops (McLeish et al, 2018; Conti et al, 2017). Plant viruses use elaborate ways to suppress or evade host defence machinery to ensure their survival (Wang, 2015; Pallas and Garcia, 2011).
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