Botanical Bio-Warfare: How Plants Stop Pathogens

On the surface, plants look like easy targets. After all, they can't move, they don't have an immune system like we do, and they are constantly at the mercy of wind, rain, UV radiation, herbivores, and microbial pathogens , and that's all on a good day! If we were rooted in place in such an exposed habitat, we wouldn't stand a chance; yet, plants grow and thrive in most places despite these challenges, suggesting that they're much tougher than they look. In fact, it turns out that plants have a variety of defensive strategies that are amazingly efficient at preventing and overcoming infection.

Figure 1.

Figure 1.

Guarding the gates: pre-existing defenses

If an ounce of prevention is worth a pound of cure, as the old adage goes, then a plant's first defense is to avoid making itself vulnerable. One might not think it, but a plant's surface is actually engineered to keep out unwanted guests. Most of us have had the occasional unpleasant encounter with a rose's thorns, or a nasty case of poison ivy, but these are just two examples of a wide variety of defenses plants deter would-be attackers. In fact, most exposed plant tissues are made up of tough, lignified cell walls coated with a layer of waxy cuticle, which forms a virtually impenetrable barrier to most pathogens. The leaf surface is so tough that many successful pathogens have actually had to evolve special strategies for penetrating the leaf. Others rely on stealth, slipping in unnoticed through open stomata or through sites that are already damaged.

Once the leaf surface has been compromised, plants rely on a variety of chemical defenses to halt the attack.

"Many plants use secondary metabolites as pre-formed antimicrobials, and there is good genetic evidence that some of these may be major determinants of resistance," says Dr. Richard Dixon, director of the Plant Biology division of the Noble Foundation in Ardmore, Oklahoma. These "phytoanticipins," as the name suggests, are low-molecular weight antimicrobial compounds that are produced constitutively in anticipation of a pathogen encounter and allow a plant to fight off an infection while other, slower defensive strategies are brought into play.

Sounding the alarm: pathogen recognition and induced defenses

Although pre-existing barriers and chemical defenses may hold an invader at bay for a short time, recognition of a pathogen attack is critical to a plant's overall survival strategy. Plants recognize many clues that they are under attack and respond accordingly. Such "elicitors" of plant defenses include plant and fungal cell wall components, bacterial glycoproteins, viral capsid proteins, and microbial avirulence proteins. Avirulence proteins are produced by plant pathogens and are necessary for a pathogen to infect a plant. But, as Dr. Igor Kovalchuk, a plant biologist at the University of Lethbridge in Alberta, Canada, explains, these same proteins that make pathogens infectious also sound the alarm to plants:

"Plants have evolved a system to recognize avirulence proteins, which tells the plant that it is under attack and that it needs to do something about it," he says.

Recognition of avirulence proteins by plants forms the basis of "gene-for-gene" plant resistance, where the compatibility of the plant-pathogen interaction is decided based on the matching of dominant genotypes (Figure 2). If a plant possesses the dominant resistance (R) gene corresponding to the pathogen's dominant avirulence gene (Avr), then the interaction is said to be incompatible, and no disease develops. Alternatively, if the plant possesses no matching R gene for a pathogen's avirulence gene, then the interaction is compatible and the infection proceeds. If we think of the pathogen's Avr proteins as a type of "key" that gains them access to a plant, then in an incompatible interaction, we can think of the plant's matching R gene as blocking access to the keyhole, which keeps the pathogen from gaining a foothold. In a compatible interaction, the keyhole is left unprotected, and the pathogen can simply let itself in and make itself at home.

Figure 2. Host-pathogen recognition. If a plant has the appropriate R gene to correspond to the pathogen's Avr gene, then the plant is resistant and no disease develops. If, however, the plant does not have the matching R gene, the interaction may result in infection.

Figure 2. Host-pathogen recognition. If a plant has the appropriate R gene to correspond to the pathogen's Avr gene, then the plant is resistant and no disease develops. If, however, the plant does not have the matching R gene, the interaction may result in infection.

An R-Avr recognition event initiates a signaling cascade, which often results in a hypersensitive response and development of systemic resistance. The hypersensitive response is characterized by the collapse and death of tissue immediately surrounding the site of infection, often resulting in the appearance of brown spots on the leaf, which we sometimes recognize as a symptom of disease. In fact, this type of self-sacrifice by the plant is an attempt to contain the pathogen and prevent the infection from spreading throughout the plant. If a plant is particularly efficient at thwarting its attacker, this hypersensitive cell death may only involve one or a few cells and no outward sign of infection is apparent. This is probably why the vast majority of the plants we encounter look healthy, despite the fact that they are constantly exposed to various pathogens and other forms of stress.

The hypersensitive response may also be accompanied by the localized accumulation of another type of defensive secondary metabolite. "Phytoalexins commonly accumulate following an hypersensitive response in the area around the lesion," says Dixon. Phytoalexins are similar to phytoanticipins in that they are low-molecular weight antimicrobials, but unlike phytoanticipins, phytoalexins are produced only during a pathogen attack, and tend to remain localized at the site of infection since they may actually be toxic to the plant. Because phytoalexins are non-specific, their role in plant defense may be particularly important in a plant's initial fight against a virulent pathogen (i.e., a pathogen for which the plant has no corresponding resistance gene). "I suspect that the broad non-host resistance that is the norm in plant-microbe interactions is often the result of the activity of natural products, although this is difficult to dissect genetically as several pathways may be involved," Dixon explains. Transgenic plants expressing phytoalexins from other species have been shown in some cases to be more resistant to pathogens. For example, when resveratrol, a phytoalexin common in grapevine and peanut, was expressed in alfalfa, Dixon said, "The plants gained resistance to leaf spot fungus." Other similar experiments with tobacco, rice, and other species have also produced promising results, raising hopes that we may be able to improve a plant's own natural defenses against stress and disease.

Calling in reinforcements: Acquired resistance and the development of R-genes

Once a single cell recognizes that an attack has occurred, it releases a chemical messenger, salicylic acid, which triggers the onset of a plant-wide resistance known as systemic acquired resistance (SAR). SAR provides broad-spectrum protection against further infection lasting as long as several weeks. Another signaling molecule, jasmonic acid, is believed to cause another type of systemic resistance known as the induced systemic resistance (ISR), in response to wounding from herbivores or infection by root-colonizing microbes. These induced responses put the plant on guard against a subsequent infection.

Figure 3. Pathogen-induced genome rearrangement in tobacco. Leaf A was treated only with buffer, while leaf B was infected with tobacco mosaic virus. The glowing spots represent cells in which homologous recombination has occurred. (Source: Kovalchuk Lab, University of Lethbridge)

Figure 3. Pathogen-induced genome rearrangement in tobacco. Leaf A was treated only with buffer, while leaf B was infected with tobacco mosaic virus. The glowing spots represent cells in which homologous recombination has occurred. (Source: Kovalchuk Lab, University of Lethbridge)

But what happens if a plant does not have the appropriate resistance gene to mediate all of these defense responses? Is the plant doomed to decimation because of this vulnerability? Maybe not, according to Kovalchuk, whose recent research may have uncovered a mechanism by which plants can develop new resistance genes. Kovalchuk has found that tobacco plants infected with the tobacco mosaic virus show elevated levels of homologous recombination, a repair mechanism for DNA strand breaks and a measure of genome stability (Figure 3). His studies indicate that this pathogen-induced genetic shuffling may provide opportunities for plants to develop new resistance genes, similar to the way recombination in the mammalian major histocompatibility complex results in the generation of new antibodies in our own immune system. "Although there are fundamental differences in the way mammals and plants respond to pathogen attack, we have evidence that a similar system for generating new alleles exists in plants and have developed protocols to elucidate how it operates," he explained. Kovalchuk is working to uncover the signaling pathway involved in this response, which he calls the systemic recombination signal, to determine how this recombination response fits in relation to other plant defense responses

Plants: not as helpless and boring as you thought

OK, so they can't run and they can't scream (or, at least, we can't hear them), but that doesn't mean plants can't fight back. They have an elaborate defense system to protect themselves from pathogens and environmental stress , so the next time you stop to sniff the flowers, remember , they may look pretty, but they're not pushovers!


Further Reading

Baker, B et al. (1997). Signaling in plant-microbe interactions. Science. 276:726-733.

Clergeot, P et al. (2001). PLS1, a gene encoding a tetraspanin-like protein, is required for penetration of rice leaf by the fungal pathogen Magnaporthe grisea. Proc.Natl.Acad.Sci.USA. 98:6963-6968.

Dixon, RA. (2001). Natural products and plant disease resistance. Nature. 411:843-847.

Hain, R et al. (1993). Disease resistance results from foreign phytoalexin expression in a novel plant. Nature. 361:153-156.

Hammerschmidt, R. (1999). Induced disease resistance: how do induced plants stop pathogens? Physiol.Mol.Plant Pathol. 55:77-84.

Kobayashi, S et al. (2000). Kiwifruits (Actinidia deliciosa) transformed with a Vitis stilbene synthase gene produce piceid (resveratrol-glucoside). Plant Cell Reports. 19:904-910.

Kovalchuk, I et al. (2002). Pathogen-induced systemic plant signal triggers DNA rearrangements. Nature. 423:760-762.

Stark-Lorenzen, P et al. (1997). Transfer of a grapevine stilbene synthase gene to rice (Oryza sativa L). Plant Cell Reports. 16:668-673.

Vanetten, H et al. (1994). Two classes of plant antibiotics: phytoalexins versus "phytoanticipins". The Plant Cell. 11911-1192.

JYI has received funding support from several sources, including the Burroughs Wellcome Fund, the National Science Foundation, and Duke University.
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