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  • Botany Notes On – Physiology Of Parasitism – For W.B.C.S. Examination.

    Plant disease is the abnormal growth and development of a plant. A diseased plant is incapable of carrying out its normal physiological functions to the best of its genetic potential. Individual parasite or pathogen strains infect some host strains more readily than others causing diseases in such hosts.Continue Reading Botany Notes On – Physiology Of Parasitism – For W.B.C.S. Examination.

    This may be due to the production of virulent factor(s) that is/are specific to that particular host variety by such a pathogen or due to the presence of some essential nutrients needed by the pathogen in the host variety (Hammond-kosack et al., 2003).

    Specificity has to do with both the factors that determine virulence in the pathogen and also those that confer resistance in the host. Pathogen virulence and host resistance may both be determined by more than one factor. Most pathogens exhibit a high degree of host-specificity. Non-host plant species are often said to express non-host resistance (Jones et al.,2006T).

    The term host resistance is used when a pathogen species can be pathogenic on the host species but certain strains of that plant species resist certain strains of the pathogen species. There can be overlap in the causes of host resistance and non-host resistance. Pathogen host range can change quite suddenly if, for example, the capacity to synthesize a host-specific toxin or effector is gained by gene shuffling/mutation, or by horizontal gene transfer from a related or relatively unrelated organism (Friedman et al.,2007).

    Good knowledge of specificity in plant diseases is important in controlling of plant diseases caused by pathogens either through producing specialized chemicals which will attack the structural integrity or metabolic activities of these pathogens or through better techniques for breeding and deploying resistant crops.

    Host–pathogen specificity means that the relative infectiousness of a pathogen to different host strains will vary from strain to strain inthe pathogen. In a simple two-strain system, for example, one pathogen strain might infecthost strain 1 more readily than host strain 2, while the other pathogen strain mightinfect host strain 2 more readily than host strain 1. Similarly, one pathogen strain might betwice as infectious as the other to host strain 1, but four times as infectious as the other tohost strain 2. In cases like these, the rate of disease transmission will be specific to eachcombination of host and pathogen strains, in a way that cannot be expressed as the simpleproduct of each pathogen’s overall infectiousness (to all host strains) and each host’s overallsusceptibility (to all pathogen strains) (Borowicz et al., 1991).

    The genetic basis of this strong specificity is explained by the gene-for-gene elicitor-receptor model. This model takes into account a virulence (avr) genes in the pathogen which are homologous to the resistance (R) genes in the host plant. A complementary combination of avr and R genes results in an incompatible host-pathogen interaction (rejection) and triggers defense mechanisms in the host cells. By contrast, a non-complementary combination of avr and R genes (compatible) results in infection (Clarke, D.D. 1997).

     A group of genes has been implicated consisting of the hypersensitivity reaction (HR) and pathogenicity (hrp) genes which control the capacity of pathogens to develop HR in non-host plants. The transcription of hrp genes is controlled by a hostsystem. A second group of genes, the avirulence (avr) genes, code for most of the virulence-associated proteins introduced into the host cell by the type III secretion system controlled by the HRP system, and trigger programmed plant defense responses such as HR (De Wit, 1997).

    Host–pathogen specificity is widespread in nature, but little is known about its impact on the evolution of virulence. A simple host–parasite model was used to explore how the fitness consequences of pathogen infectiousness and lethality are influenced by the genetic specificity of host–parasite interactions (Kirchner et al., 2002).

    The analysis is based on a variant of the host–pathogen model developed by Kirchner and Roy (2001). The model contains two host strains and two pathogen strains. The model can be generalized straightforwardly for more complex systems. The equations assume haploid genetics for the hosts and pathogens. Thus, the equations are formally equivalent to those for ecological competition between separate host and pathogen species and could be used in that context as well. In the model, uninfected host populations are denoted Xi, where = 1 . . . 2 denotes the host strain. Infected host populations are denoted Yik, where denotes the host strain and = 1 . . . 2 denotes the pathogen strain that it is infected. The pathogens cannot survive without hosts, so they need not be modelled explicitly; instead, their dynamics are represented by the infected host population. All of the host populations are expressed as fractions of the carrying capacity.

    In specific host-pathogen interactions, the invading pathogen usually produces a toxin which affects the host normal metabolic processes. These toxins are called host-specific toxins (Kirchner et al., 2002).

    These are low molecular weight compounds which are injurious to plants. Their production is usually triggered off when a virulent strain of a pathogen infects a particular susceptible host strain.  An example of such a toxin is Victorin which is isolated from Helminthosporium victoriae, the cause of blight disease in Oats. The fungus was especially virulent on one known variety known as Victoria. Although the pathogen was particularly localized in the basal portion of the plant, symptoms extended into the leaves which often collapsed. This shows that the toxin is mobile within the plant and thus acted at a distance from the actual site of infection. Victorin is a peptide linked to a tricyclic amine and it does not affect resistant Oat cultivars (Dickson et al.,1982).

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