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1 Department of Biological Sciences, National University of Singapore, 14 Science Drive 4, Kent Ridge, Singapore 117543
2 Temasek Life Sciences Laboratory, 1 Research Link, Singapore 117604
Correspondence
Sek-Man Wong
dbswsm{at}nus.edu.sg
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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A supplementary table showing primers used in this study is available in JGV Online.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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). The 3' UTR has many roles in the virus life cycle, including regulating translation expression (Gallie & Walbot, 1990; Gallie & Kobayashi, 1994; Qu & Morris, 2000; Guo et al., 2001; Koh et al., 2003; Holden & Harris, 2004; Shen & Miller, 2004), providing a telomeric function (Dreher et al., 1989; Rao et al., 1989), facilitating viral systematic movement (Chen et al., 2003), mediating virus assembly (Choi et al., 2002) and functioning as a subgenomic RNA promoter (Haasnoot et al., 2002; Olsthoorn et al., 2004; Sivakumaran et al. 2004; Li & Wong, 2006). Therefore, given the great variation in complexity and structure of the 3' UTRs of various viruses, it is evident that various elements within the UTRs have evolved to accommodate a wide range of virus-specific requirements for infection.
The 3' termini of viral genomes contain promoters for minus-strand synthesis (Buck, 1996) and their primary sequence and/or higher-order structures play vital roles in replication (Dreher & Hall, 1988; Lin et al., 1994; Havelda & Burgyan, 1995; van Rossum et al., 1997; Chapman & Kao, 1999; Cheng et al., 2002; Wang & Wong, 2004; Hardy & Rice, 2005). Another major role of 3' UTRs is to provide specific binding sites for virally encoded RNA-dependent RNA polymerase (RdRp) subunits, and the 3' UTRs probably also interact to recognize one or more host factor(s) to generate a holoenzyme complex that participates in synthesis of minus-strand RNAs (Dreher, 1999). Although the structure of the 3' UTR is postulated to have important host-specific effects on replication of individual viruses, such putative effects and their basis have not been well documented.
Turnip crinkle virus (TCV) is a member of the genus Carmovirus, family Tombusviridae, and has been developed into one of the well-characterized models for studies of the replication of plus-strand RNA viruses (Buck, 1996; Simon, 1999). The TCV 3' UTR is 253 nt long and does not possess a poly(A) tail or form a tRNA-like structure, but contains a G/C-rich segment at the 3' terminus, of which 29 out of 33 nt are either G or C residues (Carrington et al., 1989). More recent analyses have shown that this G/C-rich segment forms a 27 nt hairpin that is terminated by a six-base single-stranded tail (Song & Simon, 1995). The hairpin is also conserved near the 3' end of the TCV satellite (sat) RNA C and several other carmoviruses (Song & Simon, 1995). This hairpin is an essential component of the sat-RNA C minus-strand promoter, and its significance for sat-RNA C accumulation has been demonstrated (Song & Simon, 1995). In addition, the TCV 3' UTR has been shown to enhance virus translation (Qu & Morris, 2000), but its role in virus replication has not been studied in detail. In this paper, we investigated the role of the primary sequence and structure of the 3' UTR in TCV replication in protoplasts of two different hosts, Hibiscus cannabinus L. and Arabidopsis thaliana (L.) Heynh. The results reveal substantial differences in the requirements of the 3' UTR for replication in protoplasts of these two plants.
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METHODS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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). The primers used in this study are listed in Supplementary Table S1 (available in JGV Online). To facilitate construction, a mutant (pTCV-XhoI) was first generated by overlapping PCR to introduce a unique XhoI restriction-enzyme site at position 3798 of the TCV cDNA. A series of deletion mutants, designated p3820/4050, p3850/4050, p3881/4050, p3922/4050 and p3947/4050, was constructed as follows. Five PCR amplifications were performed using the forward primers UTR-3820, -3850, -3881, -3922, -3947 and reverse primer 3' TCV-XbaI. The resulting PCR products were digested with XhoI and XbaI and inserted into XhoI–XbaI-digested pTCV-Xho. Using a similar strategy, another three mutants, p3983/4050, p4002/4050 and p4018/4050, were constructed by using the forward primer 5' TCV-2358 and the reverse primers UTR-3983, -4002 and -4018 for fragment amplification. These PCR products were digested with BamHI–XbaI and ligated into pTCVt1d1 that had been treated with BamHI and XbaI. These constructs were used to define the 3' UTR requirements for TCV replication in Hibiscus and Arabidopsis protoplasts. To analyse the secondary structure of the 27 nt hairpin near the 3' terminus of the viral RNA, nine mutants, pH-DEL, pUS, pUS-1, pUS-2, pLS, pLS-1, pLS-2, pL-EXC and pL-DEL, were constructed by PCR amplification using the primers designated for structural analyses (see Supplementary Table S1, available in JGV Online) and the resulting PCR fragments were digested with BamHI and XbaI and inserted into pTCVt1d1.
Transfection of protoplasts and Northern blot analysis.
Hibiscus (Liang et al., 2002) and Arabidopsis Col-3 (Damm & Willmitzer, 1991) protoplasts were transfected with 10 µg infectious RNA produced by in vitro transcription (MEGAscript T7; Ambion). Total RNA was extracted from inoculated protoplasts at 24 h post-inoculation (p.i.) and analysed by Northern blot hybridization. A probe complementary to nt 2740–3798 of the TCV genome was prepared with a DIG labelling mix (Roche) and used for detection of virus accumulation. The intensities of RNA bands were measured by using a GS-710 calibrated imaging densitometer (Bio-Rad). The accumulation level of each mutant was quantified as the ratio of the intensity of the genomic RNA to that of the corresponding 28S rRNA, and normalized to that for pTCVt1d1. Each mutant was evaluated in at least two independent experiments.
Prediction of RNA secondary structure.
RNA MFOLD version 2.3 from http://www.bioinfo.rpi.edu/applications/mfold (Zuker, 2003) was used to predict the secondary structure of each mutant RNA.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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), so we created a TCV mutant lacking 149 nt (nt 3798–3946) at the 5' extremity of the 3' UTR (Fig. 1a). Interestingly, accumulation of this mutant, named p3947/4050, could not be detected in Hibiscus protoplasts (Fig. 1b), but replicated to wild-type (wt) levels in Arabidopsis protoplasts (Fig. 1c). These results indicate that the 149 nt sequence is critical for TCV accumulation in Hibiscus protoplasts, but is dispensable in Arabidopsis protoplasts. Thus, the requirements for elements within the 3' UTR sequence for TCV accumulation are host-dependent.
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) and transcripts were transfected individually into Hibiscus protoplasts. Northern blot analyses showed that the accumulation of these TCV mutants increased gradually as the deletion sizes decreased. The accumulation of p3922/4050 and p3881/4050 (Fig. 2b, lanes 3 and 4), which have deletions of 124 and 83 nt, respectively, was <5 % of the levels occurring in protoplasts transfected with wt TCV transcripts. However, the levels of p3850/4050 (Fig. 2b, lane 5), with a deletion of 52 nt, increased to 31 % of the wt levels, and those of mutant p3820/4050 (Fig. 2b, lane 6), with a 22 nt deletion, increased to 72 % of the wt levels. Therefore, in Hibiscus protoplasts, the minimal 3' UTR essential for detectable levels of TCV accumulation encompassed nt 3922 to the end (nt 4050) of the genome. However, to reach wt levels of accumulation, the full-length 3' UTR sequence was required.
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). Transfection of the transcripts from these three mutants into Arabidopsis protoplasts revealed that the accumulation of each mutant was comparable to that of the wt virus (Fig. 2c). Therefore, we conclude that, in contrast to Hibiscus protoplasts, 33 nt at the 3' terminus is sufficient to maintain virus accumulation at wt levels in Arabidopsis protoplasts, whereas other parts of the 3' UTR sequences are dispensable.
Structural requirements of the 27 nt hairpin for TCV accumulation
The 33 nt region at the 3' terminus of TCV RNA consists of a 27 nt hairpin followed by a six-base single-stranded tail (Fig. 3a), as has been predicated previously (Song & Simon, 1995). Deletion of this hairpin, but not the 3'-terminal 6 nt, resulted in failure of TCV to accumulate to detectable levels in both Hibiscus and Arabidopsis protoplasts (Fig. 3b), indicating that the hairpin sequences are essential for TCV accumulation in both hosts.
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). In Hibiscus protoplasts, TCV accumulation was not detected when the base pairing of either the upper stem (mutants US-1 and US-2; Fig. 3c, lanes 3 and 4) or the lower stem (mutants LS-1 and LS-2; Fig. 3c, lanes 6 and 7) was disrupted. However, mutants US and LS (Fig. 3c, lanes 2 and 5), whose base pairing was restored by compensatory mutations, accumulated to levels comparable to those of wt TCV (Fig. 3c, lane 1). Deletion of the loop abolished virus accumulation (mutant L-DEL; Fig. 3c, lane 9), but changing the sequence of this loop to its complement (mutant L-EXC; Fig. 3c, lane 8) reduced accumulation to approximately 80 % of the wt level. These results indicate that, in Hibiscus protoplasts, the stem of the 27 nt hairpin, but not the specific nucleotide sequence, is essential for TCV accumulation. In addition, the loop structure within the hairpin is required for virus accumulation and its structure appears to be more important than its sequence.
In Arabidopsis protoplasts, the accumulation levels of the compensatory mutants, including US, LS and L-EXC (Fig. 3d; lanes 2, 5 and 8), were comparable to those of wt TCV (Fig. 3d, lane 1) and these results were consistent with the data obtained from Hibiscus protoplasts. Surprisingly, other mutants (US-1, US-2, LS-1, LS-2 and L-DEL) containing disruptions of the upper stem or lower stem, or a deletion of the sequence of the loop (Fig. 3d; lanes 3, 4, 6, 7 and 9), which failed to accumulate in Hibiscus protoplasts, reached approximately 50–60 % of wt TCV levels in Arabidopsis protoplasts. These results indicate that, in Arabidopsis protoplasts, the structure of the upper stem, lower stem and loop are of minor importance for TCV accumulation, and that changes in the nucleotide sequence have only minimal, if any, effects.
Effects of the 27 nt hairpin on TCV accumulation are host-dependent
Based on the accumulation levels in Hibiscus and Arabidopsis protoplasts, the mutants were divided into two groups (Fig. 4). Group I mutants (US, LS and L-EXC) accumulated to high levels in both host protoplasts. The 27 nt hairpin was maintained in all mutants within this group, but the calculated free energy indicated that the structure of each mutant was approximately 4 % less stable than the wt TCV structure. Group II mutants (US-1, US-2, LS-1, LS-2 and L-DEL) were able to accumulate in Arabidopsis protoplasts, but not in Hibiscus protoplasts. The hairpin mutants were significantly less stable than the wt virus, except for mutant LS-2 (Fig. 4, Group II). All of the mutants in this group had loops and stems of variable lengths and sequences, some of which affected the length of the single-stranded region at the 3' ends of the RNAs. These results suggest that there is a strict requirement of the 27 nt hairpin for TCV accumulation in Hibiscus protoplasts, whereas in Arabidopsis protoplasts, variation within the hairpin structure can be accommodated and the structural requirement is more flexible. Therefore, the 27 nt hairpin affects TCV accumulation in a host-dependent manner.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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; Dreher, 1999). Despite substantial progress in understanding the significance of 3' UTRs on virus replication, essentially little information is available about the role of the primary sequence and/or higher-order 3' UTR structures in virus accumulation in different hosts. Herein, we have described a host-dependent effect on TCV accumulation that requires both primary-sequence and secondary-structural elements of the 3' UTR. In this study, only the 33 nt sequence at the 3' terminus of TCV RNA is required to maintain the accumulation of mutant virus to wt levels in Arabidopsis protoplasts, whereas the full-length 3' UTR is essential for virus accumulation in Hibiscus protoplasts.
In animal viruses, deletion of a portion of the 3' UTR in three flaviviruses, dengue virus type 4, Tick-borne encephalitis virus and Kunjin virus, suppresses virus replication by disrupting or reshaping the conserved secondary structure of the 3' UTR, rather than by loss of sequence motifs (Proutski et al., 1999). These results lead us to postulate that the internal 220 nt of the TCV 3' UTR may serve as a spacer to maintain accurate conformation of the core promoter element and/or facilitate core element interactions with the TCV RdRp complex in Hibiscus protoplasts. However, the 3' UTR sequence also contributes to RdRp complex assembly and stimulates replicase activity in several viruses (Quadt et al., 1995; Panaviene et al., 2004, 2005). Therefore, it is possible that internal components of the TCV 3' UTR may act to recruit host factor(s) into the RdRp complex and assist complex assembly specifically in Hibiscus protoplasts. The 3' UTR of carmoviruses has been implicated in translation of viral proteins (Qu & Morris, 2000; Koh et al., 2002). In addition, the uncapped viruses in the family Tombusviridae seem to contain a translation enhancer in their 3' UTRs (Batten et al., 2006; Kneller et al., 2006; Scheets & Redinbaugh, 2006). Thus, it appears that the internal 220 nt of the TCV 3' UTR may harbour the essential element(s) required for efficient translation of viral RdRp in Hibiscus protoplasts. Regardless of possible mechanisms, our results demonstrate that the 3' UTR sequence has a host-dependent function that affects TCV accumulation. Similar results have been reported for the poliovirus 3' UTR, which demonstrates a cell-dependent role in replication of this virus. With its entire 3' UTR deleted, the accumulation level of the poliovirus mutant is reduced slightly in HeLa cells, but decreased significantly in a neuroblastoma cell line (Todd et al., 1997; Brown et al., 2004).
In TCV, a potential base pairing between 5'-GGGC-3' (nt 3987–3990) and 5'-GCCC-3' (nt 4047–4050) is thought to support asymmetrical synthesis of plus- and minus-strand RNA (Zhang et al., 2004). This type of RNA–RNA interaction is considered to be prevalent in members of the family Tombusviridae, in which a replication-silencer element (RSE) contained in the 3' UTR is able to base pair with the 3'-complementary silencer sequence (3' CSS) at the 3' end of the genomic RNA (Na & White, 2006). However, our results for the 33 nt of the TCV 3' UTR seem to challenge the notion that the conserved interaction of RSE with 3' CSS is essential in regulating virus replication.
The hairpin near the 3' terminus is conserved in several carmoviruses and in some satellite agents associated with these viruses (Song & Simon, 1995). In TCV, the 3'-terminal 27 nt hairpin is absolutely required for virus accumulation in both Hibiscus and Arabidopsis protoplasts. Hence, it was of interest to determine the extent to which permutations in the structure affect replication in these two hosts. Therefore, we compared the accumulation levels and stability of several hairpin mutants with those of wt TCV and have shown that the wt 27 nt hairpin is better adapted than the mutants for replication in Arabidopsis protoplasts. These results are reminiscent of a previous study in which TCV sat-RNA C mutants containing modifications in a 3'-terminal 23 nt hairpin retained biological activity in turnip plants (Stupina & Simon, 1997). However, subsequent in vivo SELEX (systematic evolution of ligands by exponential enrichment) selections have shown that the wt 23 nt hairpin is optimal for sat-RNA C accumulation in turnip plants (Carpenter & Simon, 1998).
Several studies in animal viruses have shown that manipulation of the 3' UTR can have host-specific effects on replication. In West Nile virus, introduction of an extra bulge into a long stem–loop at the 3' UTR greatly enhances virus replication in mosquito cells, but has no effect in mammalian cells (Yu & Markoff, 2005). Moreover, changes in the secondary structure of the 5' terminus of Sindbis virus have more pronounced effects on virus accumulation in mosquito cells than in mammalian cells (Fayzulin & Frolov, 2004). In addition, in Tomato bushy stunt virus (TBSV), mutation of 1 or 2 nt within a putative cis-acting element can alter host specificity (Scholthof & Jackson, 1997). Therefore, as a general working hypothesis, alterations of secondary structures in viral genomes can influence virus replication differently in various hosts and these activities may lead to specific selection effects within these hosts. Similar host-dependent models have also been described in subviral agents, including Cucumber mosaic virus satellite RNA (Sleat & Palukaitis, 1992) and Potato spindle tuber viroid (Wassenegger et al., 1996; Qi & Ding, 2002).
In addition to analyses of virus-specific components that affect replication, a series of host proteins involved in virus replication have been characterized (Lai, 1998). By developing yeast as a model, host proteins that affect replication of Brome mosaic virus (Kushner et al., 2003) and a TBSV defective interfering RNA (Panavas et al., 2005) have been identified by using genome-wide screening assays. Several host factors that are thought to be components of RdRp complexes have been identified (Lai, 1998; Serva & Nagy, 2006). These studies have greatly enhanced our knowledge of host biochemical activities that have roles in virus replication. However, the mechanisms whereby the primary and secondary structures of the 3' UTR and other cis-acting elements of these viruses interact with host components are obscure. In TCV, one model is that replication in Arabidopsis versus Hibiscus protoplasts may require different host factors or differentially interacting host-factor alleles that mediate stringent host-dependent requirements for replication. Identification and comparison of such factors in Arabidopsis and Hibiscus remain a focus of our laboratory, and we hope to elucidate the requirements for interactions of the host-specific components with various elements of the TCV 3' UTR.
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ACKNOWLEDGEMENTS |
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Received 5 September 2006;
accepted 25 October 2006.
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