Host-Pathogen Interaction PN Sharma Department of Plant Pathology CSK HPKV, Palampur-176062
PATHOGEN DEFENCE IN PLANTS A BIOLOGICAL AND MOLECULAR VIEW Two types of plant resistance response to potential pathogens : the non-host resistance response (frequent): non-host resistance (basic incompatibility) is exhibited by all plant species that respond to potential pathogen without apparent R\avr gene combinations. the race\cultivar- specific host resistance response (comparatively rare). It is genetically defined by the direct or the indirect interaction between the product of a dominant or Semidominant major plant resistance gene (h) the Complementary product of the Corresponding dominant pathogen avirulence (avr) gene. Thus, the presence or absence of race cultivar-specific resistance in a given host is dependant on the genotypes of the interacting partners Apart from this distinction the biochemical process occurring in host & non host resistance are very similar.
BASIC INCOMPATIBILITY (Basic Resistance) heterologous PATHOGEN No genes expressed needed For pathogenecity, hence No colonization of the plant feasible No interaction ( or only interaction towards expression of active basic resistance) non-host PLANT Non susceptible to pathogen attack, unfit for becoming parasitized FIRST LEVEL of pathogen defense (Prell & Day,2000)
Inducible plant defense reactions: active basic resistance and race specific resistance PLANT PATHOGEN active basic resistance, non- host plant resistance, mechanism pathogen non specific, and determined by many different genes SENSOR signal recognition leads to race specific resistance, host plant resistance, the resistance gene originates from mutation, effective only against particular pathogen races race specific resistance factor (receptor) SENSOR SIGNAL (general elicitor) SIGNAL (Specific elicitor) pathogenecity genes, adapted to one single or several plant species Pathogenecity factors triggering of defense reactions, effective against different pathogens avirulence gene produces the signal recognized by the resistant host plant Avirulence factor (specific elicitor) gene for gene recognition leading to conditional expression of resistance Only to pathogen races with a corresponding avirulence gene, expressed as HR (Prell & Day,2000)
STEPS IN PLANT- PATHOGEN INTERACTION PERCEPTION SIGNALLING RESPONSE
PERCEPTION Perception means how pathogen and host recoginize each other. It may take place directly or indirectly. After evaluation of numerous physiological, biochemical and genetic experiments, different models have gained importance as the basis for all models is the gene-for-gene relationship between host and pathogen for triggering racespecific resistance. Direct interaction models Indirect interaction models
Mechanisms responsible for triggering Race specific resistance The recognition process during the interaction between host and the pathogen represents a Signal- Sensor reaction i.e. a signal or elicitor is released from the pathogen and is received by the sensor or receptor located, most probably on the surface of the host cell. The elicitor is the avirulence product (A) where as receptor (sensor) is the resistance factor. The ensuing recognition event between them generate a signal transduction pathway that ultimately affect the sites (s) of the plant cells that are responsible for activating defense reaction.
Gene for gene hypothesis does not address the actual nature of the process, structure and substances participating in the signal transduction. After no. of physiological, biochemical and genetic experiments, four models have been proposed to demonstrate the nature of recognition reaction and the expression of the defense reaction: The Elicitor- Receptor model The Dimer Model The Ion Channel defense model The Suppressor- receptor model. The basis for all the four model is gene-for- gene relationship between host and the pathogen for triggering race specific resistance
Each model is derived from different underlying concepts & experiments The elicitor receptor model is based on physiological and biochemical experiments The Dimer model applies to the expts of elicitor- receptor model a stringent and formal genetic interpretation that refer to genetic regulation in bacteria.
The Ion Channel defense model departs from electro and membrane physiological experiments by introducing into the discussion membrane bound ion channels combined with receptor for elicitors, enzyme complexes and second messengers which together form signal transduction chain that can alter the metabolic activities of the plant cell. The suppressor- receptor model refers to the same experimental results of elector- receptor model but interpret them using different assumptions.
Elicitor-Receptor Model (Albersheim et al., 1981) This hypothesis involve the two gene group system of plant genes, where one gene act as a sensor within the signal-sensor reaction that help in pathogen recognition Second group of several genes that express the plant defense reactions However, this model does not explain how the recognition by the plant turns on expression of the plant dense genes.
According to E-R model, the release of race specific resistance proceeds as follows; The pathogens Avr either directly produces a signal or the Avr gene encodes an enzyme that produces an elicitor from pathogen material. The plant recognition of the exogenous elicitor of race specific resistance i.e. sensor, receptor and resistance factor is genetically determined by the race specific genes. Since each resistance factor recognizes only one corresponding avirulence factor and specific elicitor one speaks of a pair of corresponding R and Avr genes determining race specific resistance. The plant receptor is presumed to be a membrane protein localized in plasma membrane so this location of receptor close to cell wall may provide an earleiest meting point between elicitor and receptor.
The minimal functions assigned to receptors that recognizes specific elicitors are: Extra cellular binding of the ligand, the signal, which on a molecular level is the first step towards recognition between specific elicitor & its receptor Transmission of the signal generated to the internal membrane surface by binding between the ligand and its receptor. Activation by the transmitted signal of the socalled Effectors. (the effectors covers all induced processes leading to the expression of defense genes in the plant nucleus.
R Avirulence factor Recognition Membrane protein receptor (Albersheim et al., 1981)
ELICITOR-RECEPTOR-model Signal gene (pathogen) Signal (elicitor) RECOGNITION Sensor (receptor) Sensor gene (plant) Cytoploasmic membrane Avr R Avirulence factor? Membrane proteins receptors Resistance factor RELEASE of expression of defense genes, active defense by plants (Prell & Day,2000)
Elicitor- receptor Model Pathogen Avr Gene ELICITOR R Gene Plant Resistance Responses incl. the HR Gabriel and Rolfe (1990)
However, the elicitor receptor model specifies neither the structure of the corresponding receptor nor does it define the nature and mechanism of action of the effectors. Thus in summary, the race specific resistance triggered in this way manifests itself in metabolically active cells through the expression of active defense reactions induced by the particular Effector. The defense is exhibited in two ways: HR (PCD) Activation of genes that develops/ creates new defense barrier in the plants.
Dimer Model Given by Ellingboe 1982. It is based on the hypothesis that Avr product and R-gene product form a dimer ie, single gene in the host and single gene in pathogen form a product made up of two gene products. Dimer acts as a negatively acting regulator directly blocking the expression of genes leading to the establishment of basic compatibility, hence to parasitism. Dimer acts as a genetic regulator at the level of transcription.
The products of the avirulence and resistance genes that form dimer were proposed to consist: either of the corresponding mrnas, the translated proteins of both genes or one mrna and one translated protein of each one of the portion. There was also the possibility that the dimer consisted of 2 primary gene products bound to particular site on the DNA, or that from the dimer some regulatory active molecule is cleaved of it. Once the basic compatibility is blocked by the dimer basic resistance is restored.
Dimer model is in contrast to E-R model which assumes that hew defense mechanism are established by the host plant in the presence of basic compatibility. The dimer was also proposed to release Hypersensitive cell death, but no mechanism for this function was proposed. The restoration of defense mechanism belonging to basic resistance by the action of dimer may be called as reactivated defense.
There are two main differences between the dimere and E- R modle The dimer model is based on the idea that the defense mechanisms of basic resistance are re activated by the regulatory action of the dimer where as in E-R model, new defense mechanism are established in the presence of basic compatibility. The specific recognition between avirulence and resistance factor give rise to dimer which act as a genetic regulator directly at the DNA level, however, in E-R model, after specific recognition at the cell membrane additional reaction chains release the expression of defense genes in th ecell nucleus. In other words the pathogen defense or incompatibility according to the dimer model is believed to result from a block of reaction chains involved in basic compatibility or pathogenicity, whereas the E-R model regards incompatibility as the establishment of new defense mechanism in the presence of already existing basic compatibility.
Avr R Avirulence factor Dimer Regulator molecule (Ref: Ellingboe, 1982)
ION CHANNEL MODEL Gabriel,1988 It gives emphasis on the interaction between elicitor and resistance gene product from more or less immediate effect on gene expression to the epigenetic level. This level represents network of signal transduction process that regulate metabolic activities by either activating or blocking gene expression, permanently or transiently. It assumes that trans-proteins located at the cell surface, some of which function as ion channels, provide all the steps necessary for triggering race specific resistance. Thus, the same system provide not purely pathogen recognition but also for the transduction of signals involved in pathogen defense.
Inspired by findings obtained from electrophysiological experiments on plants and other organisms. These experiments showed that electrical membrane potential ion concentration in cytoplasm are key elements in the signal transduction. In plants membrane bound ion pumps plants crucial role in maintaining concentration gradients between the all interior and exterior Ca2+ ions play important role in controlling transcription activation. A small increase in Ca2+ concentration in cytoplasm activate transcription and other metabolic processes. Hence, integrity of plasmalemma and tonoplast are of vital importance for all its metabolic activities.
Another reason for proposing this model was plants subjected to stress such as chemical wounding or infection or due to pathogen toxin or effectors, loss of electrolytes from the affected cell or tissue. First response is efflux of or leakage of K+ Ions. The loss of electrolytes and membrane depolarization results from recognition event associated with the pathogen attack that ends in hypersensitive response.
Avr opening of channels R Avirulence factor Closed transmembrane channels (Ref: Gabriel,1988 )
Recognition between specific elicitor, the Avr product of pathogen and its corresponding transmembrane protein result in plant to trigger the opening of trans-membrane protein linked to ion channels thereby opening of channel leads to efflux of K + to Cl -. Influx of H+ to Ca 2+ the so called K + /H + response depolarization. Complete membrane disintegration leads to instant cell death but local impairment could liberate signals which would diffuse into neighboring cells inducing stress reaction in them. Intensity of the signals triggered by recognition between elicitor to trans-membrane protein depends upon (i) size and number of ion channel, (ii) Binding intensity to membrane proteins (iii) Magnitude and speed of substance exchange through the cell membrane.
Basic ion channel defense model was further modified by speculation about the nature of function of transmembrane proteins. Three kinds of membrane proteins: a. Highly conserved: receptors e.g. cellular Recognize endogenous b. Less well conserved: Recognize exogenous receptors originating from pathogen e.g. chitin, glucose. c. Non-conserved: Recent in evolutionary origin. Recognize environmental avirulence factor, host selective toxin.
SUPRESSOR RECEPTOR MODEL Model was extended by Bushnell and Rowell (1981) and Heath (1982). It is based on the fact that all plants are susceptible to attack of any pathogen and hence plant exhibit basic compatibility. However, basic compatibility is conteracted by a general elicitor produced by all pathogen which releases unspecific basic resistance. In order to colonize a particular plant the homologous pathogen has to produce specific suppressor to block the action of general elicitor i.e. pathogen blocks secondarily its own elicitor of basic resistance. It assumes that active basic resistance is triggered unspecifically by general acting elicitors produced by all pathogens is like wise recognized by receptors present in all plants.
However, part pathogen become compatible with certain plant species because of mutation, the pathogen produces a species specific suppressor that prevents its general elicitor from acting on plant receptor or block elicitor receptor interaction in other way, disturbing subsequent signal transduction, or hindering formation or action of effector. In short, basic resistance would be prevented by specific suppressor produced by pathogens thus allowing basic compatibility thus Bailey described this as elicitor/specific suppression, to counteract to the release of active basic resistance by a specifically acting elicitor.
(Ref: Bushnell, 1981)