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Random Plant Viral Variants Attain Temporal Advantages During Systemic Infections and in Turn Resist other Variants of the Same Virus.

Zhang XF, Guo J, Zhang X, Meulia T, Paul P, Madden LV, Li D, Qu F - Sci Rep (2015)

Bottom Line: Finally, SLs of TCV-infected plants became highly resistant to secondary invasions of another TCV variant.The leading variants then colonize large areas of SLs, and resist the superinfection of lagging variants in the same areas.In conclusion, superinfection resistance is the primary driver of random enrichment of viral variants in systemically infected plants.

View Article: PubMed Central - PubMed

Affiliation: Department of Plant Pathology , Ohio Agricultural Research and Development Center, The Ohio State University, 024 Selby Hall, 1680 Madison Ave, Wooster, 44691, US.

ABSTRACT
Infection of plants with viruses containing multiple variants frequently leads to dominance by a few random variants in the systemically infected leaves (SLs), for which a plausible explanation is lacking. We show here that SL dominance by a given viral variant is adequately explained by its fortuitous lead in systemic spread, coupled with its resistance to superinfection by other variants. We analyzed the fate of a multi-variant turnip crinkle virus (TCV) population in Arabidopsis and N. benthamiana plants. Both wild-type and RNA silencing-defective plants displayed a similar pattern of random dominance by a few variant genotypes, thus discounting a prominent role for RNA silencing. When introduced to plants sequentially as two subpopulations, a twelve-hour head-start was sufficient for the first set to dominate. Finally, SLs of TCV-infected plants became highly resistant to secondary invasions of another TCV variant. We propose that random distribution of variant foci on inoculated leaves allows different variants to lead systemic movement in different plants. The leading variants then colonize large areas of SLs, and resist the superinfection of lagging variants in the same areas. In conclusion, superinfection resistance is the primary driver of random enrichment of viral variants in systemically infected plants.

No MeSH data available.


Related in: MedlinePlus

Exclusion of a TCV variant by its pre-inoculated relative is highly specific.(A) Mutual exclusion between sequentially inoculated variants A and I in N. benthamiana plants. (B) Lack of exclusion between TCV variant A and CarMV. Sequential inoculations were performed as described earlier, except here the N. benthamiana plants were used as hosts. Northern blot hybridizations were carried out to distinguish the various virus variants.
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f4: Exclusion of a TCV variant by its pre-inoculated relative is highly specific.(A) Mutual exclusion between sequentially inoculated variants A and I in N. benthamiana plants. (B) Lack of exclusion between TCV variant A and CarMV. Sequential inoculations were performed as described earlier, except here the N. benthamiana plants were used as hosts. Northern blot hybridizations were carried out to distinguish the various virus variants.

Mentions: We first reproduced the mutual exclusion between TCV variants in N. benthamiana by sequentially inoculating variants A and I onto two halves of the same Nb-P19 leaves. As expected, prior inoculation with I (Fig. 4A, lanes 5 and 6) or A (lanes 7 and 8) prevented the accumulation of A or I, respectively, in the SLs of infected plants. However, similar experiments with variant A and CarMV revealed that they coexisted in the sequentially infected plants, regardless of the order of inoculation (lanes 5–8). Thus, exclusion between TCV variants likely depended on high levels of sequence identity at either nt or aa levels.


Random Plant Viral Variants Attain Temporal Advantages During Systemic Infections and in Turn Resist other Variants of the Same Virus.

Zhang XF, Guo J, Zhang X, Meulia T, Paul P, Madden LV, Li D, Qu F - Sci Rep (2015)

Exclusion of a TCV variant by its pre-inoculated relative is highly specific.(A) Mutual exclusion between sequentially inoculated variants A and I in N. benthamiana plants. (B) Lack of exclusion between TCV variant A and CarMV. Sequential inoculations were performed as described earlier, except here the N. benthamiana plants were used as hosts. Northern blot hybridizations were carried out to distinguish the various virus variants.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4612314&req=5

f4: Exclusion of a TCV variant by its pre-inoculated relative is highly specific.(A) Mutual exclusion between sequentially inoculated variants A and I in N. benthamiana plants. (B) Lack of exclusion between TCV variant A and CarMV. Sequential inoculations were performed as described earlier, except here the N. benthamiana plants were used as hosts. Northern blot hybridizations were carried out to distinguish the various virus variants.
Mentions: We first reproduced the mutual exclusion between TCV variants in N. benthamiana by sequentially inoculating variants A and I onto two halves of the same Nb-P19 leaves. As expected, prior inoculation with I (Fig. 4A, lanes 5 and 6) or A (lanes 7 and 8) prevented the accumulation of A or I, respectively, in the SLs of infected plants. However, similar experiments with variant A and CarMV revealed that they coexisted in the sequentially infected plants, regardless of the order of inoculation (lanes 5–8). Thus, exclusion between TCV variants likely depended on high levels of sequence identity at either nt or aa levels.

Bottom Line: Finally, SLs of TCV-infected plants became highly resistant to secondary invasions of another TCV variant.The leading variants then colonize large areas of SLs, and resist the superinfection of lagging variants in the same areas.In conclusion, superinfection resistance is the primary driver of random enrichment of viral variants in systemically infected plants.

View Article: PubMed Central - PubMed

Affiliation: Department of Plant Pathology , Ohio Agricultural Research and Development Center, The Ohio State University, 024 Selby Hall, 1680 Madison Ave, Wooster, 44691, US.

ABSTRACT
Infection of plants with viruses containing multiple variants frequently leads to dominance by a few random variants in the systemically infected leaves (SLs), for which a plausible explanation is lacking. We show here that SL dominance by a given viral variant is adequately explained by its fortuitous lead in systemic spread, coupled with its resistance to superinfection by other variants. We analyzed the fate of a multi-variant turnip crinkle virus (TCV) population in Arabidopsis and N. benthamiana plants. Both wild-type and RNA silencing-defective plants displayed a similar pattern of random dominance by a few variant genotypes, thus discounting a prominent role for RNA silencing. When introduced to plants sequentially as two subpopulations, a twelve-hour head-start was sufficient for the first set to dominate. Finally, SLs of TCV-infected plants became highly resistant to secondary invasions of another TCV variant. We propose that random distribution of variant foci on inoculated leaves allows different variants to lead systemic movement in different plants. The leading variants then colonize large areas of SLs, and resist the superinfection of lagging variants in the same areas. In conclusion, superinfection resistance is the primary driver of random enrichment of viral variants in systemically infected plants.

No MeSH data available.


Related in: MedlinePlus