In addition to pre – existing structural defenses, there are also pre – existing metabolic or biochemical defense mechanisms to provide defense.
- Germination or growth inhibitors on plant surfaces. Examples include onion smudge disease caused by colletotrichum circinans; resistant onion varieties produce phenolics, which diffuse out of scales and inhibit germination. Tomatoes also exude compounds that inhibit fungi germination.
- Lack of an essential nutrient required by the pathogen
- Inhibitory chemicals in plant cells. Resistant potatoes to the common scab disease, Verticillim wilt, contain high levels of chlorogenic acid in their cells.
- Site binding chemicals – if the parasite requires a specific binding site to identify the host or penetrate and the host does not provide it, infection will not occur. Also, if the host lacks a specific attachment or receptor site for as toxin then no toxic activity will occur.
Pre –existing biochemical compounds are either of a low or high molecular weight and include:
LMW – phenols and quinones, long chain aliphatic and olefinic compounds, aldehydes, unsaturated lactones, cyanogenic glycosides, saponins, terpenoids, stilbenes and glucosinolates
HMW – tannins, anti-microbial proteins and peptides, defensins, lysozyme, proteinase inhibitors and polygalacturonidase – inhibiting proteins.
If infection does occur by the parasite breaching these basal defenses the plant can respond by forming further induced defense structures both structural and metabolic. Structural defense mechanisms can restrict the spread of the invading pathogen and isolate it. These mechanisms are either at the tissue level and are known as 'Histological Defense Structures' or are at the cellular or sub-cellular level, which is known as ‘Cellular Defense Reactions.’ Histological defense structures include:
- Cork layer formation which prevents the pathogen or its toxins from spreading beyond the initial lesion and also prevent the pathogen from receiving any of the plant’s nutrients. E.g. Cork cells in sweet potato reduce Rhizopus soft rot.
- Rapid wound healing
- Abscission layer formation which is when the plant excises a portion of itself in order to benefit the rest
- Formation of tyloses which are overgrowths of the protoplasts of adjacent living parenchyma cells that extend into the xylem vessels. They are formed in response to xylem invading pathogens.
- Gum deposition in areas surrounding the most concentrated area of infection so that the pathogen becomes fully enclosed, isolated and eventually dies.
- Lignification e.g. in root cells of infected sunflowers
- Suberisation
Cellular defense structures are characterised by morphological changes occurring in the cell wall.
- Callose thickening of the cell wall
- Necrotic defense reaction achieved by the hypersensitive response. This is when infection of a pathogen stimulates the nucleus of the cell to migrate towards the pathogen and disintegrates. Meanwhile, brown granules form in the cytoplasm that spread and kill the invading organism.
Biochemical induced defense mechanisms produce toxic wound response compounds which may accumulate to very high levels after induction of an elicitor which as any compound of parasitic origin that ‘elicits’ the production of an anti – parasite compound by the host.
- Phenolics: these are general inhibitors of enzymes which are formed in response to injury or disease
- Pathogenesis related (PR) proteins which are normally present at low levels are produced at greater levels after invasion and have strong anti-microbial activity such as chitinases, B1-3 glucanases and proteinases
- Phytoalexins are non- specific biocides able to affect a wide range of organisms.
- Immunity or the ability to detoxify pathogen toxins or enzymes
- Hypersensitive response (HR): This response to infection prevents the spread of disease by causing localised cell death at the site of infection trapping the pathogen in a concentrated area of dead cells. Surrounding this necrotic lesion is a ring of cells that respond readily to secondary infection, therefore carrying out localised acquired resistance. This is the most common feature associated with adaptive host resistance.
- Systemic acquired resistance (SAR): Resistance developing at a distance from initial local lesion by increases in mainly PR-proteins.
- Systemic induced resistance (SIR): similar to SAR but is not accompanied by PR proteins.
-
Oxidative burst: O2- and H2O2 are produced in the HR which are anti microbial
- Nitric oxide (NO) production: Works with ROIs in the HR.
- Synthesis of hydroxyproline-rich glycoproteins
The mechanisms of defense have now been outlined but how the pathogen and plant interact has not. For the adaptive defense mechanisms to occur the plant must first recognise that it is infected with a parasite. The interactions between plant and pathogen are governed by very specific interactions between plant disease resistant genes (R) and pathogen avirulence genes (avr). Plant disease resistance occurs when both genes are present, active and dominant. This genetic interaction occurs by plant proteins encoded by R genes recognising specific pathogen proteins encoded by avr genes. This causes a cascade of signal transduction events to be activated which in turn activates various defense mechanisms such as the HR to halt the growth and spread of the pathogen. Individual R genes have narrow recognition capabilities and only trigger resistance when the invading pathogen expresses a corresponding avr gene. This is known as the gene- for-gene concept: ‘for each gene that confers resistance in the host there is a corresponding gene in the pathogen that confers virulence to the pathogen, and vice versa.’
When genes govern resistance to disease it is named true resistance. In the case of true resistance plant and pathogen have no compatibility due to a lack of chemical recognition or because the plant has the ability to defend itself because defense mechanisms have already been formed or activated by pathogen presence. There are various different types of disease resistance in terms of the effects of the plant and pathogen genes but in terms of the number of genes involved there are only two; polygenic and monogenic resistance.
Monogenic resistance, or as it is also known, vertical resistance occurs in plants which typically have only one or very few specific genes which are clustered at the telomeres of chromosomes. These genes are able to cause high resistance to a particular pathogen with the gene only providing resistance to one race of a pathogen. This means that if another pathogen race occurs, for example by mutation, the plant will require alternative major genes to be able to combat each race. With this type of resistance, plants are either resistant or susceptible. For this reason monogenic resistance is well-defined and easier to measure as there are no intermediate forms of resistance and therefore is sometimes called qualitative resistance
Polygenic resistance or horizontal resistance is different in that it involves several or many numbers of very varied genes which generally means that the plant has resistance to all races of the pathogen. The genes are not clustered but are spread all over the chromosome. Instead of being either of the extremes: resistant or susceptible, plants with polygenic resistance can have intermediate levels of resistance. The genes are synergistic meaning that they can add together to give higher levels resistance but this resistance never normally exceeds 70%. This makes it harder to measure and is sometimes called quantitative resistance. Even though the plant is resistant to more forms of a pathogen, monogenic resistance normally gives a higher level of resistance.
Monogenic and polygenic resistance is important to plant breeders and can be illustrated in the case of northern leaf blight in corn. This fungal plant disease caused by Exserohilum turcicum has caused significant losses in Ontario and the U.S Corn Belt. Plant breeders have used resistant hybrids that have reduced the losses in yield of commercial corn but when highly susceptible corn inbreds are planted high losses continue to occur. The disease produces lesions, which spread as the disease progresses. There are 4 races of northern leaf blight and most corn hybrids now have resistance to the most common races occurring in Ontario. To control the disease, corn breeders have incorporated monogenic and polygenic resistance. Monogenic Ht resistance is not able to resist all of the fungal races which is a way of indicating when a new race has developed as hybrids with the Ht gene are likely to become susceptible is new races occur. Polygenic resistance provides resistance to all races but this resistance is not as high as monogenic resistance with the level of resistance varying between hybrids.
As well as true resistance, a plant can be resistance to disease by ‘apparent resistance’ which is where susceptible plants do not become infected by either escaping disease or by being apparently tolerant to it. Disease escape can occur when one or more of the three necessary factors for disease: susceptible host, virulent pathogen and suitable environment do not occur at the same time or for enough time. For example, a plant may only be susceptible at a particular time in its life cycle. Therefore, if the pathogen is not present at that specific time the plant will escape disease. Pythium, powdery mildews and most viruses and bacteria affecting younger tissues and plants to a greater extent than older ones illustrate this. Abiotic factors such as temperature and soil moisture have also seen to have an affect on plant susceptibility with high temperature and low soil moisture favouring the escape by plants of diseases caused by Pythium and Phytophthora. Tolerance to disease is the plant’s ability to produce a good crop despite being infected with a pathogen. The plant achieves this by either lacking receptor sites for the pathogen or by being able to overcome the excretions of the pathogen.
In conclusion plants have many varied mechanisms of basal and induced resistance to parasites and pathogens and an important part of governing this resistance is by plant gene recognition of parasite genes.
References:
Agrious GN (1997)
Plant Pathology.
Academic Press. 4th Edition
Strange RN (2003)
Introduction to Plant Pathology
Wiley Press
Jackson and Taylor (1996)
Plant-Microbe Interactions: Life and Death at the Interface
The Plant Cell (1996) vol. 8 no. 10 pp1651 – 1668
De Wit P (2002)
Plant Biology: On Guard
Nature 416, 801 – 803
Odjakova and Hadjiivanova (2001)
The Complexity of Pathogen Defense in Plants
Plant Physiology 27 (1-2) 101-109
Dangl and Jones
Plant pathogens and integrated defense responses to infection
