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)

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)

PLANT Non susceptible

to pathogen attack,

unfit for becoming parasitized

“FIRST LEVEL” of

pathogen defense

heterologous non-host

(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

pathogenecity genes,

adapted to one single or

several plant species

Pathogenecity factors SENSOR

triggering of defense reactions,

effective against

different pathogens

signal recognition leads to

avirulence gene

produces the “signal”

recognized by the resistant

host plant

race specific resistance,

host plant resistance,

the resistance gene originates from

mutation, effective only against

particular pathogen races

Avirulence factor

(specific elicitor)

race –specific resistance factor (receptor)

SIGNAL

(general elicitor)

Only to pathogen races with a corresponding

avirulence gene, expressed as HR “gene for gene” recognition leading to

conditional expression of resistance

SENSOR SIGNAL

(Specific elicitor)

(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 race-

specific 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 so-called Effectors. (the effectors covers all induced processes leading to the expression of defense genes in the plant nucleus.

Avirulence factor Recognition Membrane protein

receptor

R

(Albersheim et al., 1981)

RECOGNITION Signal gene

(pathogen)

Signal

(elicitor)

Sensor gene

(plant)

Sensor

(receptor)

Avr R

Cytoploasmic

membrane

? RELEASE of expression of defense genes,

“active” defense by plants

Membrane proteins

“receptors”

Resistance factor

Avirulence factor

ELICITOR-RECEPTOR-model

(Prell & Day,2000)

Gabriel and Rolfe (1990)

Pathogen

Avr Gene

Plant

R Gene

Resistance Responses incl. the HR

ELICITOR

Elicitor- receptor Model

• 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

Dimer Regulator molecule Avirulence factor

(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 R

(Ref: Gabriel,1988 )

Avirulence factor

opening of channels

Closed transmembrane channels

• Recognition between specific elicitor, the Avr product of pathogen and its corresponding trans-membrane 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 Ca2+

– 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: Recognize endogenous

receptors e.g. cellular

• 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)