Complete resistance

vertical resistanceHighly specific (race

specific)Involves evolutionary genetic interaction

(arms race)between host and one species of pathogen

QUALITATIVE

Partial Resistance

horizontal resistanceNot specific- confers

resistance to a range of pathogens

QUANTITATIVE

ResistanceInherent capacity of a host plant to prevent or retard the development of an infectious

disease

Gene-for-Gene theory of Complete Resistance

Pathogen has virulence (a) and avirulence (A) genes

A a

Plant has resistance gene

RR rr

If the pathogen has an Avirulence gene and the host a Resistance gene, then there is no infection

Gene-for-Gene theory of Complete Resistance

The Avirulence gene codes for an Elicitor molecule or protein controlling the synthesis of an elicitor

The Resistance gene codes for a receptor molecule which ‘recognises’ the Elicitor

A plant with the Resistance gene can detect the pathogen with the Avirulence gene

Once the pathogen has been detected, the plant responds to destroy the pathogen.

Once the pathogen has been detected, the plant responds to destroy the pathogen.

.

Gene-for-Gene theory of Complete Resistance

What is an elicitor?It is a molecule which induces any plant defence response.It can be a polypeptide coded for by the pathogen avirulence gene, a cell wall breakdown product or low-molecular weight metabolites. Not all elicitors are associated with gene-for-gene interactions.What do the Avirulence genes (avr genes) code for? They are very diverse!

In bacteria, they seem to code for cytoplasmic enzymes involved in the synthesis of secreted elicitor. In fungi, some code for secreted proteins, some for fungal toxins.

Specific resistance to a plant disease is based on what is called gene-for-gene recognition, because it depends on a precise match-up between a genetic allele in the plant and an allele in the

pathogen.This occurs when a plant with a specific

dominant resistance alleles (R) recognizes those pathogens that possess complementary avirulence (Avr) alleles.

Specific recognition induces expression of certain plant genes, products of which defend against the pathogen.

If the plant host does not contain the appropriate R gene, the pathogen can invade and kill the plant.

There are many pathogens and plants have many R genes.

Gene-for-Gene theory

Resistance occurs if the plant has a particular dominant R allele that corresponds to a specific dominant Avr allele in the pathogen.The product of an R gene is probably a

specific receptor protein inside a plant cell or at its surface.

The Avr gene probably leads to production of some “signal” molecule from the pathogen, a ligand capable of binding specifically to the plant cell’s receptor.

The plant is able to “key” on this molecule as an announcement of the pathogen’s presence.

This triggers a signal-transduction pathway leading to a defense response in the infected plant tissue.

Gene-for-Gene theory

Disease occurs if there is no gene-for-gene recognition because (b) the pathogen has no Avr allele matching an R allele of the plant, (c) the plant R alleles do not match the Avr alleles on the pathogen, or (d) neither have recognition alleles.

Gene-for-Gene theory

Even if a plant is infected by a virulent strain of a pathogen - one for which that particular plant has no genetic resistance - the plant is able to mount a localized chemical attack in response to molecular signals released from cells damaged by infection.

– Molecules called elicitors, often cellulose fragments called oligosaccharins released by cell-wall damage, induce the production of antimicrobial compounds called phytoalexins.

Gene-for-Gene theory

Elicitors of VirusesCoat proteins, replicases, transport proteins

Elicitors of Bacteria40 cloned, 18-100 kDa in size

Elicitors of FungiSeveral now cloned- diverse and many unknown function

Elicitors of NematodesUnknown number and function

ELICITORSElicitors are proteins made by the pathogen avirulence genes, or the products of those

proteins

Kinase

Signal transduction([Ca2+], gene expression)M

embr

ane

Leucine-rich receptor

Elicitor

Transmembrane domain

Plant CellCell Wall

Model for the action of Xa21 (rice blight resistance gene)

Plant Defense Response

3 aspects of response:

1. Hypersensitive2. Local3. Systemic

Compatible interaction diseaseIncompatible interaction resistanceCompatible interaction diseaseIncompatible interaction resistance

R-Avr recognition andhypersensitive response

Avirulentpathogen

Systemic acquiredresistance

Signal transductionpathway

Hypersensitiveresponse

Acquiredresistance

Signal

Signaltransduction

pathway

4Before they die, infected cells release a chemical signal, probably salicylic acid.

3 In a hypersensitiveresponse (HR), plantcells produce anti-microbial molecules,seal off infected areas by modifying their walls, and then destroy themselves. This localized responseproduces lesions and protects other parts of an infected leaf.

2 This identification

step triggers a

signal transduction

pathway.1 Specific resistance

isbased on the binding

of ligands from the pathogen to receptors in plant cells.

5 The signal is distributed to the rest of the plant.6 In cells remote from the infection site, the chemicalinitiates a signal transductionpathway.

7 Systemic acquiredresistance isactivated: theproduction ofmolecules that helpprotect the cellagainst a diversityof pathogens forseveral days.

HR (hypersensitive response)

• Host membrane changes– oxygen radicals (H2O2, -OH) and nitrous oxide– excessive oxidation of polyphenols– signal transduction molecules activated– Lipoxygenases

• Rapid accumulation of phytoalexins and pathogenesis-related proteins at infection site = decreased pathogen multiplication

• Membrane collapse (releases antimicrobial substances and denies biotrophs the necessary living substrate)

Rapid localized necrosis of invaded tissue that accompanies containment of pathogen

Hypersensitive Response

The hypersensitive response– Causes cell and tissue death near the

infection site– Induces production of phytoalexins and

PR proteins, which attack the pathogen– Stimulates changes in the cell wall that

confine the pathogen

Local responses

Cessation of cell cycle Induction of genes that promote resistance

– Phenylpropanoid pathway induced: products include salicylic acid (secondary inducer: induces other pathogenesis-related proteins), lignins (cell wall), and flavonoids

– Pathogenesis-related (PR) proteins– Phytoalexins increased

Fortification of cell walls with lignin, hydroxyproline-rich glycoproteins (HRGPs), etc.

Systemic Acquired Resistance

Inducer inoculation

3 days to months,then inoculate

Local acquired resistance

Systemic acquired resistance

SAR- long-term resistance to a range of pathogens throughout plant caused by inoculation with inducer inoculum

Systemic Acquired Resistance (SAR)

It is a set of generalized defense responses in organs distant from the original site of infection

It is triggered by the signal molecule salicylic acid (which activates plant defenses throughout the plant before infection spreads)

Involves gene activation and a transmitted signal.Genes induced:

chitinasesβ 1,3- glucanasesother PR proteins