Like animals, plants have a number of ways of protecting themselves against disease. Their first line of defense is their outer layer of tissue—the epidermis or cork—which is generally covered with a barrier of waxes, cutin, or suberin. However, if a pathogen, such as a virus, bacterium, or fungus, penetrates this barrier, the plant responds by producing other protective molecules. Plants and pathogens have evolved together such that pathogens have mechanisms to attack and penetrate plants, and plants have evolved mechanisms to kill the pathogens and limit the infection.
Plants and their pathogens have coevolved. As a result, plants have a system for recognizing pathogens and defending against them, preventing widespread infection. A wide range of molecules, called elicitors, trigger the plant's defenses.
Some elicitors, such as components of bacterial flagella or fungal cell walls, are common to a wide variety of pathogens, and their recognition results in a form of immunity called general immunity. These elicitors are called pathogen-associated molecular patterns (or PAMPs). PAMPs are recognized by transmembrane receptors called pattern recognition receptors (PRRs).
When certain pathogenic enzymes attack the plant cell wall, the breakdown products are also recognized as elicitors by membrane receptors.
Some elicitors, called effectors, are part of a second form of immunity—specific immunity. These effectors include pathogen-produced molecules that enter the cell. Once inside the cell, effectors bind to cytoplasmic receptors called R proteins. Hundreds of R genes, which code for the R proteins, have been identified. If a plant has the right R gene to match a particular effector, it will be immune to the pathogen.
When molecules bind to the plant receptors, the receptors become activated and trigger a cascade of reactions, culminating in changes in gene expression. As a result, the plant begins to produce a class of molecules called phytoalexins. Phytoalexins are usually phenolics or terpenes, and a cell produces them within hours of the onset of infection. These molecules can kill a variety of invading pathogen species.
Some of the genes that are expressed code for proteins called pathogenesis-related (PR) proteins. Some PR proteins kill bacteria or fungi by breaking down their cell walls. Others travel through intercellular passageways, called plasmodesmata, and serve as alarm signals to neighboring uninfected cells.
When a plant encounters a pathogen, one of its first responses is to produce additional polysaccharides, as well as a cell wall protein called extensin. These macromolecules not only reinforce the mechanical barrier formed by the cell wall, but also block the plasmodesmata, limiting the ability of viral pathogens to move from cell to cell. The polysaccharides also serve as a base on which lignin may be laid down. Lignin enhances the mechanical barrier, and the toxicity of lignin precursor chemicals makes the cell inhospitable to some pathogens.
Many signaling pathways and plant responses are shared between general and specific immunity, although in the latter these responses are accelerated and amplified. Furthermore, specific immunity usually leads to a form of programmed cell death called the hypersensitive response. In the hypersensitive response, infected cells essentially commit suicide, producing a patch of dead tissue, called a necrotic lesion, that walls off the pathogen.
In both general and specific immunity, the infected cells also send hormonal signals to the rest of the plant, stimulating a systemic response, called systemic acquired resistance. This defensive response is initiated by the plant hormone salicylic acid.
Salicylic acid is transported from the infected tissue to the rest of the plant body. Salicylic acid induces cells throughout the plant to produce PR proteins, which then lie in wait to kill any pathogens that might enter the plant. These PR proteins immunize the plant against a variety of pathogens, not just the pathogens that triggered the response. Systemic acquired resistance may last as long as an entire growing season.
The presence of a pathogen can trigger immune responses in plants. The pathogen produces molecules that serve as "elicitors." Within the plant, elicitors bind to plant receptors, and then the activated receptors initiate a cascade of events that culminates in changes in gene expression. These changes are protective to the plant.
In one protective response, the plant produces polysaccharides that plug the plasmodesmata between cells and prevent viral pathogens from moving freely from one cell to the next. The polysaccharides also enter plant cell walls and provide a foundation for the laying down of lignin, which enhances the mechanical barrier.
The plant also produces phytoalexins and PR proteins, both of which destroy a variety of pathogens.
The plant may also respond with a hypersensitive response, in which the infected region commits suicide and walls off the pathogen from infecting other parts of the plant. During this hypersensitive response, the infected region produces salicylic acid, a molecule that may then be transported throughout the plant. Salicylic acid triggers the widespread production of additional PR proteins, which provide the plant with systemic acquired immunity.