Sense and Antisense RNA-Mediated Resistance to Potato Leafroll Virus in Russet Burbank Potato Plants

Kawchuk, L. M.

doi:10.1094/mpmi-4-247

Cited by 115 publications

(46 citation statements)

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“…However, the extreme variation between individual plants and the frequent lack of correlation between gene expression levels and the degree of resistance (Kawchuck et al, 1991 ;Lindbo & Dougherty, 1992) has made it difficult to compare directly the efficacy of each strategy. We have attempted to circumvent this problem by using protoplasts for replication assays that mimic the constitutive expression of a viral inhibitor, and by ensuring that the molar ratio of the interfering construct to the viral genome is strictly defined at the outset of inoculation.…”

Section: Discussionmentioning

confidence: 99%

Interference with brome mosaic virus replication by targeting the minus strand promoter

Huntley

Hall²

1993

Journal of General Virology

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Sense and antisense strategies for interfering with the replication of brome mosaic virus (BMV) were examined. The effects of 200 nucleotide-long sense and antisense transcripts, corresponding to the viral 3' end (-) strand promoter, on the accumulation of progeny viral RNAs were studied by co-inoculation with wildtype BMV RNAs. Progeny accumulation in barley protoplasts transfected with either sense or antisense transcripts of the (-) strand promoter and BMV RNAs-1 and -2 was decreased by more than 90 %, and by 60 to 80 % when RNA-3 was also present. This trans interference was concentration-dependent, and reduced both (+) and (-) strand progeny accumulation to a similar extent. The appearance of complementary (-) strands indicated that sense interfering transcripts could serve as templates for (-) strand synthesis, and the use of deletion mutants revealed that the observed interference was in part mediated by this template activity. The reproducibility of the protoplast assay used here allows rapid evaluation of interference strategies and comparisons to be made of alternative approaches to engineered resistance. The results presented here suggest that targeting viral (-) strand promoters with sense and antisense transcripts may be an effective method for engineering plant resistance to viral infection.

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Section: Discussionmentioning

confidence: 99%

Interference with brome mosaic virus replication by targeting the minus strand promoter

Huntley

Hall²

1993

Journal of General Virology

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“…We can now add to these "classic" cases of CPMP several recent examples, particularly among members of the aphidtransmitted potato virus Y (PVY; potyvirus) and luteovirus (PLRV) groups, and the thrip-transmitted TSWV, where intentionally truncated, antisense or nonexpressing (-AUG) CP genes have been transformed into plants and have provided measurable protection or even complete immunity against the appropriate parent virus (50)(51)(52)(53)(54)(55)(56)(57)(58). Recent field tests with the untranslatable tobacco etch virus (TEV) CP RNA lines (50,51) have shown 100%o resistance to high disease pressure (W. G. Dougherty, personal communication).…”

Section: On Cp-mediated Protection and Proposed Mechanismsmentioning

confidence: 99%

“…Recent field tests with the untranslatable tobacco etch virus (TEV) CP RNA lines (50,51) have shown 100%o resistance to high disease pressure (W. G. Dougherty, personal communication). In all these cases (50)(51)(52)(53)(54)(55)(56)(57)(58), it may be that some direct form of RNA-RNA interference between the transgene transcript and the challenge virus (especially the low titer PLRV) could account for the resistant phenotype. However, with the truncated TEV CP transgenic plants, it was common for the inoculated leaves to develop symptoms and virus titers similar to control plants, but for the plant to outgrow the infection.…”

Section: On Cp-mediated Protection and Proposed Mechanismsmentioning

confidence: 99%

Strategies to protect crop plants against viruses: pathogen-derived resistance blossoms.

Wilson¹

1993

Proc. Natl. Acad. Sci. U.S.A.

229

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Since 1986, the ability to confer resistance against an otherwise devastating virus by introducing a single pathogen-derived or virus-targeted sequence into the DNA of a potential host plant has had a marked influence on much of the research effort, focus, and shortterm objectives of plant virologists throughout the world. The vast literature on coat protein-mediated protection, for example, attests to our fascination for unraveling fundamental molecular mechanism(s), our (vain) Despite extensive and sometimes elegant experimentation, the molecular mechanism(s) of this viral "crossprotection" have remained elusive and controversial. In some cases, the coat protein (CP) of the protectant virus was thought to be primarily responsible, either by preventing particle disassembly or by re-encapsidating the incoming genome of the more severe challenge virus. However, viroids [240-to 380-nt-long, naked circular single-stranded (ss)RNA pathogens] and mutant viruses making assembly-defective or no detectable CP could also cross-protect against their more severe relatives. Such observations prompted models based on inhibitory interactions between sense and antisense RNAs or between the replicational machineries ofthe two competing pathogens (6). Controversy arose largely because available molecular technology could not resolve which regulatory or coding sequence(s) or polypeptide product(s) from the actively replicating genome of the primary (protectant) pathogen were responsible for interfering with the many replicative processes essential to establish infection by the secondary, related, and more severe virus. In contrast, multiple infections by unrelated viruses sharing a common host are very prevalent in nature. Many aspects of this older story have their parallels in current hypotheses and lack of a unified model for pathogenderived resistance in transgenic plants.The advent of improved cell and tissue culture techniques, efficient protocols for Agrobacterium tumefaciens-mediated transformation and plantlet regeneration in dicotyledonous species (7) [and more recent methods for monocot crops (8-10)], has permitted, among other applications (11,12), the theory of pathogenderived virus resistance to be tested in practice.Collaboration between researchers at Monsanto and Washington University (St. Louis) led to the first report of CPmediated protection (CPMP) against tobacco mosaic virus (TMV) in tobacco in 1986 (4). Since then, CPMP has been reported for over 20 viruses in at least 10 different taxonomic groups, in a wide 3134 variety of dicot plant species, and the list is increasing rapidly.

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“…A possible reason why other endogenous proviral sequences did not evolve as resistance mechanisms is that their expression may adversely affect important physiological processes of the host (Gavora et al, 1995a,b) (Gavora, 1990 (Hamilton, 1980) and the concept of pathogen-derived resistance was first put forward in a formal statement by Sanford and Johnston (1985). There are several approaches to the introduction of disease resistance by gene transfer in plants (Fitchen and Beachy, 1993 (Kawchuk et al, 1991) and tobacco plants and similar transcripts of tobacco mosaic virus (Powell et al, 1989 (Gerlach et al, 1987 …”

Section: Principal Elements Of Virus-host Interactionsmentioning

confidence: 99%

Resistance of livestock to viruses: mechanisms and strategies for genetic engineering

Gavora¹

1996

Genet. Sel. Evol.

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Sense and Antisense RNA-Mediated Resistance to Potato Leafroll Virus in Russet Burbank Potato Plants

Cited by 115 publications

References 0 publications

Interference with brome mosaic virus replication by targeting the minus strand promoter

Interference with brome mosaic virus replication by targeting the minus strand promoter

Strategies to protect crop plants against viruses: pathogen-derived resistance blossoms.

Resistance of livestock to viruses: mechanisms and strategies for genetic engineering

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