Abstract
Ethylene plays critical roles in plant development and biotic stress response, but the mechanism of ethylene in host antiviral response remains unclear. Here, we report that Rice dwarf virus (RDV) triggers ethylene production by stimulating the activity of S-adenosyl-L-methionine synthetase (SAMS), a key component of the ethylene synthesis pathway, resulting in elevated susceptibility to RDV. RDV-encoded Pns11 protein specifically interacted with OsSAMS1 to enhance its enzymatic activity, leading to higher ethylene levels in both RDV-infected and Pns11-overexpressing rice. Consistent with a counter-defense role for ethylene, Pns11-overexpressing rice, as well as those overexpressing OsSAMS1, were substantially more susceptible to RDV infection, and a similar effect was observed in rice plants treated with an ethylene precursor. Conversely, OsSAMS1-knockout mutants, as well as an osein2 mutant defective in ethylene signaling, resisted RDV infection more robustly. Our findings uncover a novel mechanism which RDV manipulates ethylene biosynthesis in the host plants to achieve efficient infection.
Highlights
Rice is a staple food crop in many regions, a model monocot plant for research, and a host to many viruses (Wu et al, 2015; 2017)
Our results demonstrated that ethylene biosynthesis and signaling are critical for Rice dwarf virus (RDV) infection and rice susceptibility
We found that Pns11 interacts with OsSAMS1 and enhances its enzymatic activity in vivo and in vitro (Figures 2 and 3)
Summary
Rice is a staple food crop in many regions, a model monocot plant for research, and a host to many viruses (Wu et al, 2015; 2017). RDV is transovarially transmitted by the green rice leafhopper (Nephotettix cincticeps) in a persistent-propagative manner (Cao et al, 2005; Zhou et al, 2007; Wei and Li, 2016). S1, S2, S3, S5, S7, S8, and S9, encode structural proteins P1, P2, P3, P5, P7, P8, and P9, respectively, which form double-layered virions; the remaining segments, S4, S6, S10, S11, and S12, encode the nonstructural proteins Pns, Pns, Pns, Pns, and Pns (Cao et al, 2005; Zhou et al, 2007; Liu et al, 2014; Jin et al, 2016; Wei and Li, 2016)
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