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Resistance Inherent capacity of a host plant to prevent or retard the development of an infectious disease Complete resistance Partial Resistance vertical resistance Highly specific (race specific) Involves evolutionary genetic interaction (arms race) between host and one species of pathogen QUALITATIVE horizontal resistance Not specific- confers resistance to a range of pathogens QUANTITATIVE 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. Gene-for-Gene theory 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. ELICITORS Elicitors are proteins made by the pathogen avirulence genes, or the products of those proteins Elicitors of Viruses Coat proteins, replicases, transport proteins Elicitors of Bacteria 40 cloned, 18-100 kDa in size Elicitors of Fungi Several now cloned- diverse and many unknown function Elicitors of Nematodes Unknown number and function Model for the action of Xa21 (rice blight resistance gene) Leucine-rich receptor Transmembrane domain Elicitor Cell Wall Membrane Kinase Signal transduction ([Ca2+], gene expression) Plant Cell Plant Defense Response Compatible interactiondisease disease Compatible interaction Incompatible interactionresistance resistance Incompatible interaction 3 aspects of response: 1. Hypersensitive 2. Local 3. Systemic 4Before they die, infected cells release a chemical signal, probably salicylic acid. 3 In a hypersensitive response (HR), plant cells produce antimicrobial molecules, seal off infected areas by modifying their walls, and then destroy themselves. This localized response Signal produces lesions and protects other parts of an infected leaf. Hypersensitive response 2 This identification step triggers a Signal transduction signal transduction pathway pathway. 1 Specific resistance is based on the binding of ligands from the pathogen to receptors in plant cells. The signal is distributed to the rest of the plant. 5 6 In cells remote from the infection site, the chemical initiates a signal transduction pathway. 7 Signal transduction pathway Acquired resistance Avirulent pathogen R-Avr recognition and hypersensitive response Systemic acquired resistance Systemic acquired resistance is activated: the production of molecules that help protect the cell against a diversity of pathogens for several days. HR (hypersensitive response) Rapid localized necrosis of invaded tissue that accompanies containment of pathogen • Host membrane changes – – – – oxygen radicals (H2O2, -OH) and nitrous oxide excessive oxidation of polyphenols signal transduction molecules activated Lipoxygenases • Rapid accumulation of phytoalexins and pathogenesisrelated proteins at infection site = decreased pathogen multiplication • Membrane collapse (releases antimicrobial substances and denies biotrophs the necessary living substrate) 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, hydroxyprolinerich glycoproteins (HRGPs), etc. Systemic Acquired Resistance Inducer inoculation Local acquired resistance 3 days to months, then inoculate SAR- long-term resistance to a range of pathogens throughout plant caused by inoculation with inducer inoculum Systemic acquired resistance 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: chitinases β 1,3- glucanases other PR proteins