Abstract
Co-infection of none-coding satellite RNAs (sat-RNAs) usually inhibits replication and attenuates disease symptoms of helper viruses. However, we find that the sat-RNA of Beet black scorch virus (BBSV) and low temperature (18°C) additively enhance the systemic infection of BBSV in Nicotiana benthamiana. Northern blotting hybridization revealed a relatively reduced accumulation of BBSV-derived small interfering RNAs (siRNAs) in presence of sat-RNA as compared to that of BBSV alone. Cloning and sequencing of total small RNAs showed that more than 50% of the total small RNAs sequenced from BBSV-infected plants were BBSV-siRNAs, whereas the abundance of sat-siRNAs were higher than BBSV-siRNAs in the sat-RNA co-infected plants, indicating that the sat-RNA occupies most of the silencing components and possibly relieves the RNA silencing-mediated defense against BBSV. Interestingly, the 5′ termini of siRNAs derived from BBSV and sat-RNA were dominated by Uridines (U) and Adenines (A), respectively. Besides, the infection of BBSV alone and with sat-RNA induce down-regulation of miR168 and miR403, respectively, which leads to high accumulation of their targets, Argonaute 1 (AGO1) and AGO2. Our work reveals the profiles of siRNAs of BBSV and sat-RNA and provides an additional clue to investigate the complicated interaction between the helper virus and sat-RNA.
Highlights
The satellite RNAs of plant viruses rely on the helper virus for replication and encapsidation but share little or no sequence similarity with the helper virus genome (Murant and Mayo, 1982; Hu et al, 2009)
We found that the sat-RNA of Beet black scorch virus (BBSV) facilitated the systemic infection of the helper virus in N. benthamiana
Our results show that BBSV is temperature sensitive and the systemic infection is enhanced at lower temperature
Summary
The satellite RNAs (sat-RNAs) of plant viruses rely on the helper virus for replication and encapsidation but share little or no sequence similarity with the helper virus genome (Murant and Mayo, 1982; Hu et al, 2009). Since sat-RNA C is capable of interfering the encapsidation of TCV genomic RNAs thereby to boost the accumulation of free coat proteins, which are RNA silencing suppressor (Wang and Simon, 1999; Thomas et al, 2003; Zhang and Simon, 2003), these observations suggest that some sat-RNAs enhance helper virus disease symptoms by directly or indirectly suppressing RNA silencing. To our knowledge, there is no report to document an enhancement of helper virus titers during co-infection with sat-RNAs (Hull, 2002; Simon et al, 2004)
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