Fig. 7. Model of virus-host interactions mediated by sRNAs.

a Virus infection induces a complex regulatory matrix of bidirectional sRNA-mediated interactions at the plant:virus interface. Virus infection causes changes in the expression of miRNAs and mRNAs that may be critical in the determination of host susceptibility and resistance. Perturbations in miRNA levels may affect the amplitude and efficacy of miRNA-mediated cleavage resulting in changes in the level of their mRNA targets. Virus infection also triggers the biosynthesis of vasiRNAs from host transcripts via the formation of dsRNA intermediates. Recruitment of vasiRNAs into cleavage-effector silencing complexes provides control over a vast range of host transcripts including transcripts of the vasiRNA-producing genes and their homologs (e.g., vasiRNAs produced by CABBP1) and transcripts derived from secondary target genes (e.g., vasiRNAs produced by NBR1). The replicating virus uses dsRNA replicative intermediates to produce vsiRNAs which are competent to guide sequence-specific cleavage of both viral and host-mRNA targets. Likewise, viral RNA is an accessible target for vsiRNA-, vasiRNAs, and hsiRNA-directed cleavage. hsiRNAs are produced by the host also in the absence of virus and may contribute to basal resistance of the host. b NBR1 may function as a regulatory hub for plant - virus interactions. The NBR1 protein controls virus infection by targeting viral effector proteins (e.g. the VSR of TuMV) and viral particles for degradation by autophagy. The virus, in turn, triggers conversion of NBR1 mRNA into vasiRNAs with the potential to induce widespread control over NBR1 and other gene targets. The role of NBR1 as a virus-inducible hub for trans-acting siRNA production is feedback-controlled through the ability of the same locus to also produce vasiRNAs that target the virus.