Laboratory of Plant Pathology, Graduate School of Agriculture, Kyoto University, Kyoto 606-8502, Japan
Correspondence
Kazuyuki Mise
kmise{at}kais.kyoto-u.ac.jp
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ABSTRACT |
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These authors contributed equally to this work.
The GenBank/EMBL/DDBJ accession numbers for the sequences determined in this paper are AB183259AB183261.
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INTRODUCTION |
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Brome mosaic virus (BMV) is a positive-sense single-stranded RNA virus and the type species of the genus Bromovirus in the family Bromoviridae (Ahlquist, 1999). The genome of BMV consists of tripartite RNAs, designated RNA1, RNA2 and RNA3. RNA1 and RNA2 encode the 1a and 2a proteins, respectively, both of which are required for viral RNA replication (Kroner et al., 1989
, 1990
). RNA3 encodes the 3a protein and CP. The 3a protein is the MP of BMV, as it is essential for BMV movement (Rao, 1997
; Schmitz & Rao, 1996
; Takeda et al., 2004
). Encapsidation-competent CP is also required for BMV movement (Okinaka et al., 2001
; Rao & Grantham, 1995
, 1996
). BMV infection produces tubular structures containing virion-like particles on infected protoplasts (Kasteel et al., 1997
). Collectively, BMV is thought to move from cell to cell as virions. Most studies on BMV infection have been undertaken using particular virus strains (e.g. strain M1) derived from the Russian strain (Ahlquist et al., 1984
; Dreher et al., 1989
), although many other strains of BMV have been isolated (Lane, 1974
, 1981
).
Plant viruses in a given family generally have similar features regarding the role of CP in cell-to-cell movement. However, at least one exception to that rule is found within the family Bromoviridae; BMV, CCMV and CMV show different types of requirement for CP and move from cell to cell as distinct forms, as mentioned above (Callaway et al., 2001). On the other hand, the form of cell-to-cell movement of these viruses is altered by mutations in the C termini of MPs (Nagano et al., 2001
; Osman et al., 1999
; Takeda et al., 2004
). In CMV, truncation of the C terminus of MP confers the ability to mediate CP-independent movement (Nagano et al., 2001
). In CCMV, truncation of the C terminus of MP causes the loss of the ability to mediate CP-independent cell-to-cell movement (Osman et al., 1999
). Furthermore, a few amino acid substitutions in the C terminus of BMV-M1 MP are sufficient to alter its requirement for CP in cell-to-cell movement (Takeda et al., 2004
). Interestingly, these substitutions do not affect the long-distance movement of BMV (Takeda et al., 2004
), indicating that CP-dependent cell-to-cell movement is not a prerequisite for systemic infection by BMV. These observations led us to hypothesize that there are natural BMV strains that do not require CP for intercellular movement. In this study, to examine this hypothesis, we investigated whether the BMV MPs of five other strains mediate the cell-to-cell movement of the BMV M1 strain without CP.
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METHODS |
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Construction of cDNA clones.
Plasmids pB1TP3, pB2TP5 and pB3TP8 (transcript name, B3/M1/CP) contain full-length cDNA clones of wild-type RNA1, RNA2 and RNA3, respectively, of BMV-M1 (Janda et al., 1987). Plasmids pB1WD1, pB2WD2 and pB3WD3 (transcript name, B3/M2/CP) contain full-length cDNA clones of wild-type RNA1, RNA2 and RNA3, respectively, of BMV-M2 (De Jong & Ahlquist, 1995
). To construct pB3/KU1/GFP and pB3/M2/GFP, the 1·1 kb PstIAor51HI fragment of pB3MAR7 (transcript name, B3/M1/GFP) (Sasaki et al., 2003
) was replaced with the corresponding fragments of pBTFpCP2 (Mori et al., 1993
) and pB3WD3 (De Jong & Ahlquist, 1995
), respectively. To construct pB3M2(
CP/GFP2) (transcript name, B3M2/M2/GFP2), we first determined the 3' half of the cDNA sequence of pB3WD3 (GenBank/DDBJ accession no. AB183261 for full-length M2-RNA3 sequence) and precisely replaced the CP gene in pB3WD3 with a green fluorescent protein (GFP) gene, using the same strategy as used to generate pB3M1(
CP/GFP2) (transcript name, B3/M1/GFP2) (Takeda et al., 2004
). The ATCC47, ATCC178 and ATCC180 strains of BMV were propagated in barley plants (Hordeum vulgare cv. Gose-shikoku) and cDNA fragments containing the respective MP genes of these strains were synthesized as described previously (Sasaki et al., 2001
). The MP genes of these strains were then amplified by PCR using the appropriate primers and the amplified DNA fragments were sequenced directly by using a model 310 DNA sequencer (Applied Biosystems). DDBJ accession numbers for the MP genes of ATCC47 and ATCC180 are AB183259 and AB183260, respectively. To construct pB3/47/GFP and pB3/180/GFP, the MP gene of pB3MAR7 was precisely replaced with the MP genes of ATCC47 and ATCC180, respectively. The 0·2 kb FbaIAor51HI fragment of pB3MAR7 was replaced with the corresponding fragments of pB3/KU1/GFP, pB3/M2/GFP and pB3/180/GFP to construct pB3/D281E/GFP, pB3/S297G+T299S/GFP and pB3/L275P/GFP, respectively. pB3/E59Q+S81P/GFP, pB3/E59Q/GFP, pB3/S81P/GFP, pB3/S297G/GFP and pB3/T299S/GFP were constructed by PCR-based site-directed mutagenesis of pB3MAR7 with the appropriate primers. Plasmids to be digested with FbaI, a dam methylation-sensitive restriction enzyme, were amplified in Escherichia coli JM110. The cDNA regions derived by PCR were sequenced to confirm the presence of only the desired mutations. All cDNA plasmids were linearized with EcoRI and capped viral RNA transcripts were synthesized as described previously (Kroner & Ahlquist, 1992
). The transcript from the plasmid containing the RNA3 variant is referred to by its plasmid name without the prefix p, unless otherwise stated, as transcript names.
Analysis of viral RNAs and proteins.
Transcripts of BMV RNA3 derivatives were inoculated together with BMV RNA1 and RNA2 transcripts onto Chenopodium quinoa plants as described previously (Nagano et al., 1999). Unless otherwise indicated, all RNAs 1 and 2 used as inocula were derived from BMV-M1 only throughout this study, except for one subsection in the Results section, where transcripts from BMV-M2, as well as those from BMV-M1, were used. GFP fluorescence in inoculated leaves of C. quinoa was detected as described previously (Sasaki et al., 2003
). Tissue-print analysis to detect viral RNAs was performed as described previously (Mise et al., 1993
). Distribution of CP in the inoculated leaves of C. quinoa was detected by hammer-blot analysis as described previously (Fujisaki et al., 2003
). Accumulation of CP in the inoculated leaves of C. quinoa was examined as described previously (Takeda et al., 2004
).
In planta selection of MP mutants showing cell-to-cell movement independent of CP.
From C. quinoa leaves inoculated with B3/M1/GFP or B3/KU1/GFP, small pieces of leaf tissue that contained an infection site with multiple fluorescent cells were excised with a razor blade under an epifluorescence microscope. Progeny viral RNAs were then isolated from the collected pieces by using an RNeasy plant mini kit (Qiagen) according to the manufacturer's instructions. DNA fragments containing the MP genes of these progeny viruses were amplified by RT-PCR using the appropriate primers and the MP gene of the amplified DNA fragments were sequenced directly. To construct pB3/E262A/GFP, pB3/Q254K/GFP and pB3/44/GFP, the MP gene of pB3MAR7 was replaced with the MP genes of viruses recovered from B3/M1/GFP-inoculated leaves. To construct pB3/KU1
23/GFP, the MP gene of pB3MAR7 was replaced with the MP gene of a virus recovered from B3/KU1/GFP-inoculated leaves. To construct pB3/
23/GFP, the 0·2 kb FbaIAor51HI fragment of pB3MAR7 was replaced with the corresponding fragment of pB3/KU1
23/GFP. To construct pB3/Q254K/CP, pB3/E262A/CP, pB3/
44/CP and pB3/
23/CP, the 0·5 kb ClaIAor51HI fragment of pB3TP8 was replaced with the corresponding fragments of pB3/Q254K/GFP, pB3/E262A/GFP, pB3/
44/GFP and pB3/
23/GFP, respectively.
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RESULTS |
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As shown above, B3/S297G+T299S/GFP moved from cell to cell independently of CP, but not as efficiently as parental B3/M2/GFP (Fig. 2). The MP of BMV-M2 contains four amino acid differences from that of BMV-M1 (De Jong et al., 1995
; Table 1
), suggesting that the other two amino acid differences contribute to the altered requirement for CP in cell-to-cell movement of B3/M2/GFP. We then examined the infectivity of B3/E59Q+S81P/GFP, B3/E59Q/GFP and B3/S81P/GFP. However, all three mutants showed inefficient cell-to-cell movement (Fig. 2
). Considering these data collectively, we conclude that a single amino acid difference (S297G) in the C-terminal region of the MP of BMV-M2 contributes mainly to altering the requirement for CP in cell-to-cell movement and that the other differences in the MP of BMV-M2 also function to enhance its ability to mediate cell-to-cell movement independently of CP.
CP-defective BMV-M2 moves from cell to cell and induces necrotic local lesions in C. quinoa leaves
To confirm that MP of BMV-M2 has the ability to mediate cell-to-cell movement independently of CP in the context of the BMV-M2 genome, as well as the BMV-M1 genome, C. quinoa leaves were inoculated with RNAs 1 and 2 of BMV-M2 together with B3M2/M2/GFP2, in which the CP gene of BMV-M2 RNA3 was precisely replaced with a GFP gene. At 3 days p.i., many infection foci containing multiple GFP-expressing fluorescent cells were observed. However, because most of the infection foci contained a small cluster of necrotized cells in their centres (data not shown), we could not record the precise number of fluorescent cells. Therefore, we counted GFP fluorescence at 1 day p.i. and found many infection foci containing multiple fluorescent cells (Table 2; Fig. 3a
). At 5 days p.i., large necrotic local lesions were visible (Fig. 3b
). These results show that BMV-M2 does not require CP in either cell-to-cell movement or the induction of necrotic local lesions on C. quinoa. We also carried out genome reassortment to investigate how genomic combinations influence the CP requirement for virus movement or symptom induction. We first inoculated B3M2/M2/GFP2 onto C. quinoa with RNAs 1 and 2 of BMV-M1. Many foci with multiple fluorescent cells were observed at 1 day p.i., whereas the cell-to-cell movement of this heterologous combination was slightly slower than that of B3M2/M2/GFP2 with RNAs 1 and 2 of BMV-M2 (Table 2
). Interestingly, no necrotic local lesions were visible at 5 days p.i. on the leaves inoculated with B3M2/M2/GFP2 plus RNAs 1 and 2 of BMV-M1 (Fig. 3c
). In contrast, neither multiple fluorescent cells nor necrotic local lesions were observed after inoculation with B3/M1/GFP2, in which the CP gene of BMV-M1 RNA3 was replaced with the GFP gene, together with RNAs 1 and 2 of BMV-M2 (Table 2
; Fig. 3d
) or of BMV-M1 (Table 2
; Fig. 3e
). These results suggest strongly that RNA3 (probably the MP gene), but not RNA1 and RNA2, play a crucial role in the CP requirement in BMV movement, but that RNA1 and RNA2 are involved in the rate of cell-to-cell movement and the induction of necrotic lesions on C. quinoa.
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Spread of MP mutants in the presence of CP
To investigate the influence of the mutations identified in the in planta mutants on BMV-M1 infection in the presence of CP, four BMV RNA3 derivatives (B3/E262A/CP, B3/Q254K/CP, B3/44/CP, and B3/
23/CP) were inoculated onto C. quinoa plants together with RNAs 1 and 2 of BMV-M1. Virus infectivity was estimated by the observation of symptoms and tissue-print analysis for the detection of viral RNAs, in inoculated and upper uninoculated leaves at 14 days p.i. C. quinoa plants inoculated with wild-type BMV-M1 (B3/M1/CP) developed systemic symptoms with leaf distortions (data not shown), as reported previously (Takeda et al., 2004
). Inoculation of C. quinoa with B3/Q254K/CP or B3/E262A/CP, as well as B3/M1/CP, induced similar systemic symptoms (data not shown) and strong viral RNA signals were detected by tissue-print analysis in both inoculated and upper uninoculated leaves (Fig. 5a
). These results show that the two point mutations (Q254K and E262A) in the C-terminal region of MP of BMV-M1 have little effect on either the cell-to-cell movement of or systemic infection by BMV-M1. On the other hand, B3/
44/CP and B3/
23/CP did not induce systemic symptoms even at 14 days p.i. (data not shown), nor did they cause the accumulation of detectable amounts of viral RNA in the upper uninoculated leaves (Fig. 5a
). These results demonstrate that deletions in the C-terminal region of MP (
44 and
23) interfere with systemic infection by BMV-M1. Moreover, only weak viral RNA signals were detected in the leaves inoculated with B3/
44/CP or B3/
23/CP. To investigate virus distribution in more detail, hammer-blot analysis of those deletion mutants was performed. BMV CP was detected throughout the leaves inoculated with B3/M1/CP (Fig. 5b
), but was not detected in the leaves inoculated with B3/MP-fs/CP (Fig. 5b
), which does not express functional MP because of a frameshift mutation in the MP gene [B3B3a-FS in the paper by Takeda et al. (2004)
]. In the leaves inoculated with B3/
44/CP or B3/
23/CP, small and faint BMV CP signals were detected (Fig. 5b
). Moreover, Western blot analysis showed that BMV CP accumulated in leaves inoculated with B3/
44/CP or B3/
23/CP to levels about 50- to 100-fold lower than that accumulated after B3/M1/CP inoculation (Fig. 5c
). These results demonstrate that B3/
44/CP and B3/
23/CP moved from cell to cell in the presence of CP, but more inefficiently than did the wild-type BMV-M1.
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DISCUSSION |
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Sequence comparisons and mutational analyses of six strains of BMV demonstrated that the CP-dependent movement of BMV-M1 is controlled by MP. Furthermore, reassortment experiments further revealed that the difference in CP requirement between BMV-M1 and -M2 is attributable to RNA3, but not to RNA1 or RNA2, whereas RNA1 and/or RNA2 influences the efficiency of viral movement and the induction of host responses causing necrosis (Table 2; Fig. 3
). These data confirm the essential role of MP in determining the movement modes of BMV. Moreover, the nucleotide sequences responsible for the conversion of the CP requirement, which were identified in this study, are located mainly in the C-terminal region of BMV MP (Figs 2 and 4
), as reported previously in another system (Takeda et al., 2004
). These results reinforce the essential role of the C terminus of BMV-M1 MP in forming a functional module that is involved in the CP requirement. In support of this, recent studies in CMV (Nagano et al., 2001
), Alfalfa mosaic virus (Sánchez-Navarro & Bol, 2001
) and Cowpea mosaic virus (Carvalho et al., 2003
) have suggested or demonstrated an interaction between the C terminus of MP and the cognate CP.
We have identified several sequence changes in the MP gene that alter the requirement for CP in the cell-to-cell movement of BMV-M1 (Figs 2 and 4). How the requirement for CP is altered by such sequence changes remains unknown. However, recent studies of CMV may provide a clue to this unknown mechanism. Like BMV-M1, the Y and Fny strains of CMV require CP in cell-to-cell movement (Canto et al., 1997
; Suzuki et al., 1991
) and the requirement for CP is altered by a change in the MP sequence, i.e., deletion of the 33 C-terminal amino acids from the MPs of these CMV strains (Kim et al., 2004
; Nagano et al., 2001
). Andreev et al. (2004)
and Kim et al. (2004)
showed that the CMV MP with the 33 aa deletion binds viral RNAs more efficiently and strongly than does wild-type MP, and they suggest that CMV CP alters the MP conformation to increase its binding affinity for RNA through an indirect interaction between the two proteins. Similarly, some conformational change in the MP of BMV-M1 could be induced by the identified point mutations and deletions, leading to enhanced binding affinity for RNA and the formation of stable complexes of virus RNAs and MP. Such nucleoprotein complexes could somehow move between cells in a way distinct from the movement of virions or CP-associated complexes. Alternatively, the MPRNA complexes could escape the host defence responses that are normally blocked by CP. Further studies are required to examine these hypothetical mechanisms.
The MP of BMV-M2 has a potent capacity to mediate cell-to-cell movement independently of CP, whereas those of the five other strains examined have no ability or only a weak ability to facilitate cell-to-cell movement in the absence of CP (Fig. 2). Why does BMV-M2 MP function in a way distinct from the other MPs? A unique feature of BMV-M2 is that it systemically infects the legume cowpea line TVu-612 (Valverde, 1987
), although most known systemic hosts of BMV strains are monocotyledonous plants, such as barley. On the other hand, BMV-M1 does not systemically infect cowpea species, including TVu-612 (Mise et al., 1993
; De Jong & Ahlquist, 1995
). De Jong et al. (1995)
examined the individual and synergistic effects of four amino acid differences in the MPs of BMV-M1 and BMV-M2 (Table 1
) on local and systemic infection in TVu-612 and found that the differences enhance the rate of local and systemic infection synergistically. Interestingly, our results also show a synergistic effect of the four amino acid differences on CP-independent cell-to-cell movement (Fig. 2
). These collective and correlative data suggest that CP-independent functions of BMV-M2 MP are involved in the faster local spread and successful systemic infection of the cowpea plant and that the change in the MP sequence of BMV-M2 optimizes its infectivity of the cowpea plant. Consistent with this possibility, we have recently found other amino acid changes in BMV-M1 MP that enable BMV-M1 to move partly or fully in the absence of CP (Sasaki et al., 2005
). These amino acid changes have been identified as spontaneous mutations that allow a cowpea-non-adapted chimeric CCMV carrying the BMV-M1 MP gene to infect cowpea plants systemically (Fujita et al., 1996
; Sasaki et al., 2001
).
As shown by the MPs in BMV-M2, B3/Q254K/CP and B3/E262A/CP, as well as in some alanine-scanning mutants (Takeda et al., 2004), one or a few nucleotide substitutions are enough to convert the requirement for CP in cell-to-cell movement of BMV-M1 without affecting its capacity for long-distance movement. Of these, the MPs of B3/Q254K/CP and B3/E262A/CP appeared in planta during inoculation experiments in our greenhouse. These results imply that BMV MP mutants capable of CP-independent movement can appear in natural fields and survive by chance. Our data may also reflect a possible virus strategy in which a movement mode is selected in plant viruses, like BMV, that is between CP-dependent and -independent movements and optimizes virus infectivity of a particular range of plants. As discussed above, BMV-M2 may be an example of a strain in which a CP-independent cell-to-cell movement has been selected, allowing it to infect a leguminous plant, unlike other strains including BMV-M1.
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ACKNOWLEDGEMENTS |
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Received 23 November 2004;
accepted 13 December 2004.
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