Resistance to Plant Viruses
Some estimates put total the worldwide economic damage due to plant viruses as high as US$60 billion per year, in addition to the human costs in terms of hunger and poverty. So understanding how viruses damage plants and how this can be avoided is of the utmost importance. There are hundreds of plant-pathogenic viruses, which cause a range of diseases. However, plants have evolved elaborate and effective defence mechanisms to prevent or limit virus damage. Plants contain resistance (R) genes, which allow resistance to a range of pathogens including viruses. Each R gene gives resistance to a particular pathogen. A number of R genes have been studied in detail (Mechanisms of plant resistance to viruses. 2005 Nature Reviews Microbiology 3: 789-798). Several molecules and signalling pathways are induced on pathogen recognition, and they cooperate to produce a defensive response. Some of the best characterized of these molecules include salicylic acid, nitric oxide and reactive oxygen species, in addition to some plant hormones. RNA silencing is a highly conserved pathway in animals and plants that functions in development and in the maintenance of genome integrity. Plants have adapted this system for antiviral defences, and of course, plant viruses have in turn developed mechanisms to suppress RNA silencing. Double-stranded RNA (dsRNA) is the trigger for RNA silencing. Most plant viruses (59 of the 80-odd plant virus genera) are RNA viruses and plants have several homologues of the DICER endonuclease. These enzymes generate siRNA (short interfering RNA) as an antiviral response. So these two pathways – RNA silencing and R-gene-mediated resistance – interact to produce an effective defence response in plants.
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Having penetrated the plant cell wall, the first defence mechanism which viruses encounter are extracellular surface receptors on the host cell plasma membrane that recognize pathogen-associated molecular patterns (PAMPs). This interaction initiates PAMP-triggered immunity (PTI), which sometimes halts infection before the virus gains a hold in the plant. However, plant viruses have evolved the means to suppress PTI by interfering with recognition at the plasma membrane. Effector-triggered immunity involves the direct or indirect recognition of the virus proteins used to subvert PTI by plant R proteins (Host-Microbe Interactions: Shaping the Evolution of the Plant Immune Response. 2006 Cell 124: 803-814). Virus virulence determinants suppress the host RNA silencing response.
Genetic engineering offers a means of incorporating new virus resistance traits into existing plant varieties. The initial attempts to create transgenes conferring virus resistance were based on the pathogen-derived resistance determinants, for example, the expression of virus coat protein genes in transgenic plants was shown to induce protective effects. Since then, a large variety of virus genes encoding structural and non-structural proteins has also been shown to confer resistance to disease (Strategies for antiviral resistance in transgenic plants. 2008 Molecular Plant Pathology 9: 73-83). Subsequently, non-coding virus RNAs have been shown to be a potential trigger for virus resistance in transgenic plants, which led to the discovery of RNA silencing.
Plants have evolved a robust innate immune system that exhibits striking similarities as well as significant differences with innate immunity in animals. For example, plants are capable of perceiving PAMPs through pattern recognition receptors that bear structural similarities to animal Toll-like receptors. In addition, plants have evolved a second surveillance system based on cytoplasmic “NB-LRR” proteins (nucleotide-binding, leucine-rich repeat) that are structurally similar to animal nucleotide-binding and oligomerization domain (NOD)-like receptors. Plant NB-LRR proteins do not detect PAMPs, but recognize proteins that viruses produce in plant cells. (Molecular diversity at the plant-pathogen interface. 2007 Dev Comp Immunol)
The number of different strategies that have been developed for creating virus and viroid resistance is one of the major success stories in biotechnology. However, few of these strategies have ever been taken past the proof of principle stage in the laboratory, or small-scale field trials. The only engineered virus-resistant plants that have been grown on a large commercial scale were transformed with complete virus transgenes, and it appears that the resistance induced is of the RNA silencing type in all these cases. That means that there is still enormous potential for overcoming the detrimental effects of plant viruses through genetic manipulation of valuable plant varieties.
Tags: Agriculture, Biology, Biotechnology, Environment, Microbiology, plants, Podcast, Science, Virology
Of course, some of what makes plant viruses unique is that they often simply bypass the first line of host defence – that is, proteins associated with cell walls and cell membranes – by having transmission mechanisms that get them, as whole particles, into the cytoplasm. Any aphid- or whitefly- or trips- or leafhopper-transmitted virus, for example, gets injected directly into a cell via the piercing mouthparts of their insect vector. Viruses with blunter vehicles, such as the beetle-transmitted sobemoviruses, get into damaged cells via carriage on the surface of slicing mouthparts, and propagate in cells which manage to heal.
Another whole avenue of defence is bypassed by plant viruses which get trafficked between cells via plasmodesmata as nucleoprotein complexes, rather than as particles – a mechanism which may explain why plant viruses almost exclusively have ssNA genomes or replicative intermediates (think pararetroviruses).
See http://www.mcb.uct.ac.za/tutorial/virusentplant.htm for tall this and more!
PS: nice article; my students will be assigned it to read…B-)
Thanks Ed, so were mine ;-)