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Plants use a vast array of signals originating from micro-organisms and the environment to recognise pathogens and elicit plant defence responses. Non-specific elicitors of biotic and abiotic origin induce host defences in a broad range of host species. Abiotic elicitors such as heavy metal ions or UV light can induce stress responses in exposed tissues, which may provide an additional barrier to invading pathogens or alternatively, increase the plant's susceptibility to infection. Biotic elicitors include cell wall fragments released from fungi and bacteria, hydrolytic enzymes of plant or pathogen origin, some peptides, glycoproteins and polyunsaturated fatty acids. These elicitors induce defence responses in a range of host species. Often, non-specific elicitors act as a general indication that the cell has been damaged in some way (for example, the release of fragments of the host's own cell wall can elicit defence responses).

Specific elicitors enable defence against a very specific pathogen, and are conditioned by avirulence genes in that pathogen. Avirulence genes determine the pathogen's host range, but are only able to function in the presence of another set of genes, the 'hypersensitive response and pathogenicity' (Hrp) gene cluster. Some Hrp gene products are involved in disguising the pathogen from host recognition, thus playing a role in both virulence and avirulence.

For a biotroph to form a successful infection, it must establish a basic compatibility with its host. The pathogen may also produce compatibility factors that delay, avoid or negate recognition by a normally resistant host plant. Virulent strains appear to be able to suppress the resistance mechanisms of the host, but are not able to halt resistance responses once they are activated. Incompatibility between a host and a pathogen results in the recognition of the pathogen and activation of defence mechanisms, while compatibility results in infection.

Specific elicitors are encoded by avirulence genes, and these peptides are believed to bind to receptor peptides, encoded by host resistance genes. Recognition of the avirulence gene products by the host triggers signal transduction pathways that cause a massive shift in gene transcription and plant cell metabolism, and local and systemic signals are released that prime the rest of the plant against further infection. The presence of non-specific elicitors, such as the release of host and pathogen wall fragments, during this process may amplify the defence response.

Host-parasite specific resistance is determined by the interaction of between products of pathogen avirulence genes, Specific elicitors and products of host resistance genes. The defence responses of plants can be very rapid. Host gene expression begins within minutes, or even seconds, of exposure to elicitors or pathogens. A diverse range of elicitors can induce a common set of responses in the host, suggesting that second messengers are involved in the signalling pathway between pathogen attack and host response.



Almost every host-parasite interaction is unique in the details of the activation, localisation, timing and magnitude of the defence responses.

At the membrane

The host membrane appears to be involved in the earliest stages of pathogen recognition and signal transduction. A change in membrane permeability after exposure to a pathogen causes fluxes in ions, such as K+, H+ and Ca2+, and results in changes to gene activation and the triggering of the defence responses. Also at the membrane, the 'oxidative burst', which involves the generation of reactive oxygen species, such as hydrogen peroxide, triggers signals that affect gene expression, cross-linking in the host cell wall and initiation of later defence responses. The reactive oxygen species at the site of infection are also produced in quantities capable of killing micro-organisms directly.

At the cell wall

Preparations for the reinforcement of the cell wall, which can improve host resistance, begin very quickly after a pathogen attempts to penetrate a host cell. This is characterised by an intensification of cytoplasmic streaming and the accumulation of host cytoplasm around the site of attempted penetration. The cytoplasmic aggregates are thought to contain cellular apparatus for the synthesis of cell wall fortifications. If the host cell can repair and reinforce its cell walls quickly enough, it might reduce the penetration efficiency of the pathogen. Several types of reinforcement are produced by host cells. A papilla is a deposit of callose, silicon, lignin and proteins between the cell wall and cell membrane, directly below the point of attempted penetration, while lignitubers are lignified callose reinforcements that ensheath invading hyphal tips.

Hydroxyproline-rich glycoproteins are structural cell wall proteins involved in secondary cell wall thickening. The expression of genes governing their production is activated ahead of invading hyphae, reinforcing walls. Cross-linking of hydroxyproline-rich glycoproteins caused by the release of hydrogen peroxide in the oxidative burst also reinforces cell wall compartments. Rapid deposition of lignin and suberin following infection also increases resistance to pathogens in many plants. Lignin can also bind to hyphal tips and bacteria, physically restraining them and restricting the diffusion of their enzymes and toxins into, and the extraction of water and nutrients out of, the host cell. Cell wall reinforcements tend to be larger and more quickly formed in resistant hosts than in susceptible hosts, and inhibition of the production of callose or lignin synthesis by the pathogen enhances its penetration efficiency.

The hypersensitive response

Hypersensitive cell death is another widespread mechanism used by hosts to prevent the spread of a pathogen. Infected cells and those surrounding them "suicide", preventing further spread, and in some cases, killing the pathogen. It is often associated with the initiation of other responses, such as lignification and the synthesis of anti-microbial compounds. The success of hypersensitive cell death as a resistance mechanism depends on the nutritional requirements of the specific pathogen and the timing, magnitude and location of the host response.

Antibiotic compounds

Phytoalexins are low molecular weight antibiotics produced by many (but not all) plants in response to infection. There are many biotic elicitors of phytoalexin production, such as cell wall components, as well as abiotic elicitors, such as heavy metals and ultraviolet light. Phytoalexins inhibit the growth of bacteria and fungi in vivo and in vitro, and production of these antibiotics during an infection can induce resistance to subsequent infections by that pathogen. Over 350 phytoalexins are known in over 100 plant species. They include pterocarpans, sesquiterpenes, cryptophenols, isocoumarins, isoflavenoids, and others. Phytoalexins may be produced by any part of the plant, although different phytoalexins can accumulate in different organs. Generally, related plant species produce structurally-related phytoalexins, and many produce more than one, enabling the plant to present a toxic cocktail to invading pathogens. Phytoalexins are produced in cells surrounding an infection site and delivered to the infected cell packaged in lipid vesicles, creating a toxic micro-environment in the infected cell and, hopefully, preventing disease establishment. Phytoalexin accumulation is often associated with hypersensitive cell death, although only living cells can synthesise phytoalexins. Some plants can also sequester phytoalexins into vacuoles as stores of inactive sugar-conjugates, which can be cleaved and released quickly if initial defence responses are unsuccessful.



Delayed active defences include containment of the pathogen, wound repair, expression of pathogenesis-related proteins and the acquisition of systemic resistance. These mechanisms restrict the spread of the pathogen after infection is established and contain the damage to host tissues.

Physical responses

The ability to repair wounds can help protect the plant from further infection by other, opportunistic pathogens. A secondary meristem in fleshy tissues, fruits, roots and bark, the cork cambium, can produce cork cells, which have thick, suberised walls. These cells can create a barrier to further colonisation by the pathogen and, in some cases, develop an abscission layer around the site of infection, causing the infected tissue separate from the healthy tissue. Wounded tree trunks often secrete protective gums that seal the wound from further infection. The formation of tyloses, ingrowths if the protoplasm in xylem parenchyma can also restrict the spread of pathogenic propagules in the xylem, although they also tend to reduce the movement of water through the vessels, causing water stress in the plant.

Pathogenesis-related proteins

There is a range of novel proteins synthesised in response to infection, many of which have b-glucanase, chitinase or lysozyme activity. Some pathogenesis-related proteins disrupt pathogen nutrition. The presence of low levels of these proteins in healthy plants suggests that they might have other roles in plant growth and development aside from disease resistance. Chitinase and glucanase accumulate in the vacuoles, and glucanase is also sometimes secreted into the intercellular space. They dissolve the fungal cell wall, fragments of which then elicit hypersensitive cell death. The breakdown of the vacuole during decompartmentalisation of the cytoplasm results in a flood of hydrolytic enzymes, which have antiviral, antifungal and antibacterial activity. The accumulation of pathogenesis-related proteins peaks around 7-10 days after initial infection. The presence of these proteins before infection increases the plant's resistance to pathogens, as in the case of systemic acquired resistance.

Systemic acquired resistance

Systemic acquired resistance, or induced resistance, is characterised by the increased resistance of a plant to a wide range of pathogens following infection by one pathogen. It is therefore fundamentally different from the specific antigen-antibody mechanism of resistance seen in the immune response of mammals. Rather than providing immunity per se, systemic acquired resistance reduces the severity of later diseases. The development of systemic acquired resistance usually requires the development of a slowly expanding necrotic lesion and other localised responses to infection, the release of a phloem-translocated signal originating from the infection site, and the subsequent priming of the plant against further attacks, allowing a more rapid response in the case of future infections. The nature of the signal that triggers systemic acquired resistance is as yet unknown, and is likely to be a complex signal transduction pathway mediated by a number of stress signals. Salicylic acid plays a key role, via interaction with salicylic acid-binding proteins that can cause build-up of reactive oxygen species or activate gene expression. The levels of salicylic acid increase around necrotic lesions and remain high in plants that have acquired resistance. It is not, however, salicylic acid itself that acts as the signal that is translocated systemically throughout the plant.

Co-ordination of defence responses

The success of defence responses is increased if activated in combination. Passive mechanisms, coupled with rapid active responses and slower follow-up defences provide a broad defence front to the plant. The specific interaction between host and pathogen is of course crucial to the success of the plant's resistance or the pathogen's invasion, and is mediated by the many pathways involved in producing or detecting elicitors, enhancers, suppressors and secondary signals.


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