Hormones are tuners of plant responses to biotic and abiotic stresses. They are involved in various complicated networks, through which they modulate responses to different stimuli. Four hormones primarily regulate plant defence to pathogens: salicylic acid (SA), jasmonic acid (JA), ethylene (Et) and abscisic acid (ABA). In susceptible plants, viral infections result in hormonal disruption, which manifests as the simultaneous induction of several antagonistic hormones. However, these antagonistic hormones may exhibit some sequential accumulation in resistant lines. Virus propagation is usually restricted by the activation of the small interfering RNA (siRNA) antiviral machinery and/or SA signalling pathway. Several studies have investigated these two systems, using different model viruses. However, the roles of hormones other than SA, especially those with antagonistic properties, such as ABA, have been neglected. Increasing evidence indicates that hormones control components of the small RNA system, which regulates many processes (including the siRNA antiviral machinery and the microRNA system) at the transcriptional or post-transcriptional level. Consequently, cross-talk between the antagonistic SA and ABA pathways modulates plant responses at multiple levels. In this review, we summarize recent findings on the different roles of hormones in the regulation of plant-virus interactions, which are helping us to elucidate the fine tuning of viral and plant systems by hormones.
MATERIALS AND METHODSVirus Isolates. BaMV isolate V (BaMV-V) contains satBaMV (14). BaMV-L is an isolate derived from BaMV-V and free of satBaMV (designated as
The view that satellite RNAs (satRNAs) and satellite viruses are purely molecular parasites of their cognate helper viruses has changed. The molecular mechanisms underlying the synergistic and/or antagonistic interactions among satRNAs/satellite viruses, helper viruses, and host plants are beginning to be comprehended. This review aims to summarize the recent achievements in basic and practical research, with special emphasis on the involvement of RNA silencing mechanisms in the pathogenicity, population dynamics, and, possibly, the origin(s) of these subviral agents. With further research following current trends, the comprehensive understanding of satRNAs and satellite viruses could lead to new insights into the trilateral interactions among host plants, viruses, and satellites.
Accepted 29 October 2013. Abscisic acid (ABA) plays a key role in modulating plant responses to different biotic and abiotic stresses. However, the effect of ABA on virus infection is not fully understood. Here, we describe the effects of the ABA pathway on the accumulation of Bamboo mosaic virus (BaMV) and Cucumber mosaic virus (CMV) in two different hosts: Arabidopsis thaliana and Nicotiana benthamiana. We report that ABA2 plays a critical role in the accumulation of BaMV and CMV. Mutants downstream of ABA2 (aao3, abi1-1, abi3-1, and abi4-1) were susceptible to BaMV, indicating that the ABA pathway downstream of ABA2 is essential for BaMV resistance. The aba2-1 mutant decreased the accumulation of BaMV (+)RNA, (-)RNA, and coat protein, with the most dramatic effect being observed for (-)RNA. These findings were further validated by the use of virus-induced gene silencing and enzyme-linked immunosorbent assay in N. benthamiana. In addition, infecting N. benthamiana with BaMV or CMV increased ABA contents and activated the SA and ABA pathways, thereby disrupting the antagonism between these two cascades. Our findings uncover a novel role for ABA2 in supporting BaMV and CMV accumulation, distinct from the opposing role of its downstream genes.
Plant resistance to pathogens is tuned by defense-related hormones. Of these, abscisic acid (ABA) is well documented to moderate resistance against fungi and bacteria. However, ABA's contribution to resistance against viruses is pleiotropic. ABA affects callose deposition at plasmodesmata (therefore hindering the viral cell-to-cell movement), but here, we show that when callose synthase is down-regulated, ABA still induces resistance against infection with Bamboo mosaic virus (BaMV). By examining the potential connections between the ABA and RNA-silencing pathways in Arabidopsis (Arabidopsis thaliana), we showed that ABA regulates the expression of almost the whole ARGONAUTE (AGO) gene family, of which some are required for plant resistance against BaMV. Our data show that BaMV infection and ABA treatment regulate the same set of AGOs, with positive effects on AGO1, AGO2, and AGO3, no effect on AGO7, and negative effects on AGO4 and AGO10. The BaMV-mediated regulation of AGO1, AGO2, and AGO3 is ABA dependent, because the accumulation of these AGOs in BaMVinfected ABA mutants did not reach the levels observed in infected wild-type plants. In addition, the AGO1-miR168a complex is dispensable for BaMV resistance, while AGO2 and AGO3 were important for ABA-mediated resistance. While most ago mutants showed increased susceptibility to BaMV infection (except ago10), ago1-27 showed reduced BaMV titers, which was attributed to the up-regulated levels of AGO2, AGO3, and AGO4. We have established that ABA regulates the expression of several members of the AGO family, and this regulation partially contributes to ABA-mediated resistance against BaMV. These findings reveal another role for ABA in plants.RNA silencing provides plants with broad resistance against virus infection through small RNA (sRNA)-directed degradation (Ding, 2010). While it is well established that salicylic acid (SA) controls plant resistance to virus infection via R gene resistance (Baebler et al., 2014), it also has been suggested that SA regulates a few genes in the RNA-silencing pathway (Alamillo et al., 2006;Hunter et al., 2013). In fact, the regulation of defense responses has been demonstrated to be a hormonetuned process in many cases. Other hormones, such as jasmonic acid and ethylene, also are involved in the plant-virus interaction but exhibit specificity in terms of the infecting virus and the type of resistance triggered (Alazem and Lin, 2015).Abscisic acid (ABA) also is involved in modulating plant resistance against various pathogens, but the timing of its activation is critical for determining plant susceptibility or resistance; therefore, it has been labeled as a phase-specific modulator of defense responses (MauchMani and Mauch, 2005). Nevertheless, ABA does not seem to be phase specific against viruses, and few reports have shown that ABA improves plant resistance to viruses. We previously found that ABA treatment decreases titers of Bamboo mosaic virus (BaMV) in inoculated leaves of Arabidopsis (Arabidopsis thaliana) and that ABA-me...
The protein encoded by the first gene of the triple gene block (TGBp1) of potexviruses is required for movement of the viruses. It has been reported that single ArgRAla substitutions at position 11, 16 or 21 of TGBp1 of Bamboo mosaic virus (BaMV) eliminate its RNA-binding activity, while substitutions at position 16 or 21 only affect its NTPase activity (Liou et al., Virology 277, 336-344, 2000). However, it remains unclear whether these ArgRAla substitutions also affect the movement of BaMV in plants. To address this question, six mutants of BaMV, each containing either a single-or a double-alanine substitution at Arg-11, Arg-16 and Arg-21 of TGBp1, were constructed and used to infect Chenopodium quinoa and Nicotiana benthamiana. We found that all of the BaMV mutants were able to replicate in protoplasts of N. benthamiana. However, only the mutant with an Arg-11RAla substitution in TGBp1 remained capable of movement from cell to cell in plants. Mutants with Arg-16, Arg-21 or both Arg-16 and Arg-21 of TGBp1 replaced with alanine were defective in virus movement. This defect was suppressed when a wild-type TGBp1 allele was co-introduced into the cells using a novel satellite replicon. The ability to trans-complement the movement defect by the wild-type TGBp1 strongly suggests that the ArgRAla substitution at position 16 or 21 of TGBp1, which diminishes the RNA-binding and NTPase activities of TGBp1, also eliminates the capability of BaMV to move from cell to cell in host plants.
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