MicroRNAs control resistance to viral pathogens
The miRNA-mediated gene regulation has emerged as a novel strategy to
enhance antiviral defenses in crop plants (Ding & Voinnet 2007). Plants
have evolved different RNA silencing mechanisms to respond to diverse
classes of viral infections. Antiviral RNA silencing is triggered by
virus-derived double-stranded RNA (dsRNA) that are directly recognized
and processed by the host dicer-like proteins (DCL) to form
virus-derived small-interfering RNAs (vsiRNAs) (Baulcombe 2004). The
vsiRNAs are incorporated to the ARGONAUTE (AGO ) proteins
that form the core component of RNA-induced silencing complex (RISC).
The functional RISC either cleaves the viral RNA or arrests the viral
protein translation. Single-stranded viral RNAs require endogenous
RNA-dependent RNA polymerases (RDRs) to synthesize dsRNA that serves as
the substrate for DCLs to produce secondary vsiRNAs. To counteract the
defense response of plant, most viruses have developed specialized
proteins known as viral suppressors of RNA silencing (VSRs) that impede
the antiviral RNA silencing pathway and suppress the defense response
(Csorba, Kontra & Burgyán 2015).
MicroRNAs provide an additional layer of intrinsic defense against viral
attack. In rice, the Osa-miR528 is well characterized and known
to be involved in the regulation of defenses against the rice stripe
virus (RSV). The Osa-miR528 is sequestered away from AGO1by cleavage-defective AGO18 of rice, which is known to be
monocot-specific, upon RSV infection. This in turn prevents the
formation of functional RNA induced silencing complex. These events
further lead to the enhanced expression of downstream gene AO, which
encode for, L-ascorbate oxidase, and functions by initiating the
resistance response against RSV through enhanced accumulation of
reactive oxygen species (ROS) (Wu et al. 2017a). Further research
suggested that the transcription factor OsSPL9 specifically
regulates the expression of the Osa-miR528-AO module by binding
to the promoter of the Osa-miR528 . Mutation in the OsSPL9has been shown to cause the dramatic downregulation of Osa-miR528thereby inducing the expression of AO that leads to enhanced
resistance to RSV (Yao et al. 2019).
The AGO18 also sequester the Osa-miR168 upon RSV
infection. It has been shown that AGO18 competes with AGO1 for
binding to Osa-miR168 resulting in an elevated level ofAGO1 -mediated resistance (Wu et al., 2015). RSV invasion
triggered the expression of Osa-miR444 , which positively
regulates the immunity against viral pathogen. Transgenic plant
overexpressing the Osa-miR444 displayed a broad-spectrum
resistance to RSV by inducing OsRDR1 and silencing severalMADS box genes (Wang et al. 2016).
RSV infection perturbs the expression of Osa-miR171 . Reduced
accumulation of Osa-miR171 has been shown to severely affect
plant height and chlorophyll content and caused the RSV-like symptoms in
rice. Plants expressing miR171b were less susceptible to RSV and
attenuate RSV symptoms (Tong et al. 2017). In rice, theOsa-miR319 acts as a negative regulator of antiviral immunity
against ragged stunt virus (RRSV). Transgenic plants overexpressing theOsa-miR319 exhibit severe disease like symptoms by down
regulating target gene OsTCP21 (TEOSINTE
BRANCHED/CYCLOIDEA/PCF ) and suppressing JA-mediated plant defense
pathways (Zhang et al. 2016).