Genetics of avirulence/virulence and host specific toxins in pathogen-plant interactions Flashcards
What is the function of an avirulence allele in a GFG interaction?
Most avirulence alleles appear to encode elicitors that activate plant defenses.
What is the difference between a general elicitor and a specific elicitor?
General elicitor does not exhibit differences in cultivar sensitivity within a plant species. Examples of general elicitors are substances associated with the basic metabolism of the pathogen, e.g. cell wall glucans, chitin oligomers and glycopeptides
Specific elicitors are proteins or peptides whose production only occurs as a consequence of avirulence gene function. To fit the gene-for-gene model an elicitor must be the specific product of a pathogen avirulence gene that is recognized by the product of the corresponding resistance gene.
What is a PAMP? Give two examples of PAMPs.
Pathogen Associated Molecular Pattern
in Fungi these include chitin and ergosterol, in bacteria these include lipopolysaccharides and flagellin.
PAMPs seem to activate “basal” recognition and resistance pathways of plant defense.
Flagellin is a PAMP that is a general elicitor.
What is a type III secretion system and how is it used by bacteria during pathogenesis?
It is a common mechansism for injecting bacterial effector molecules into host cells. Genes encoding TTSS are clustered on the bacterial chromosome and often are tightly linekd with genes encoding the effector molecules. The TTSS is requierd for pathogenicity and for avirulence function in many bacteria.
What is an effector?
Effector molecules injected by Type III secretion systems can act as specific elicitors. Many of the effectors act to suppress the programmed cell death involved in HR.
What is the connection between an effector and an avirulence elicitor?
effectors can act as avirulence factors
the term effector is neutral and does not imply a negative or positive impact on the outcome, many effectors are only known by their avirulence function
Describe three strategies that can be used to identify pathogen effectors.
Biochemical approach: effector is purified from pathogen and tested for induction activity in a plant bioassay, gene is then isolated by reverse genetics
Genetic apporach: effector is isolated by map based cloning, complementation experiments or reverse genetics, elicitor activity of gene product determined using a gene expression assay
Genomics apporach: candidate effectors are first identified from sequence database and then assayed for activity using various functional assays
What is a host-selective toxin? Give two examples of HSTs.
HSTs are substances produced by a pathogenic microbe that is toxic to the hosts of that pathogen and shows little or no toxicity against non-susceptible plants. HSTs are determinants of host range or specificity. All known HSTs are produced by fungi.
Victorin (HV toxin) is one of the best.studied HSTs.It is produced by Cochliobolus victoriae, which causes foot and root rot and leaf blight of certain oat cultivars
Another well characterized HST is ToxA, a ribosomally synthesized protein produced by some wheat pathogens.
Compare the GFG models used for avirulence genes and host-specific toxins. How are they similar? How are they different? How might they be connected?
S. 88
What is apoptosis and how is apoptosis connected to host-specific toxins and GFG interactions?
Programmed cell death
Is probably important for preventing cancer and for removing diseased cells.
It differs from necrotic cell death that results from cellular damage and is needed fo normal development of most metazoans
Describe the GFG-based toxin interaction in the wheat-Pyrenophora tritici repentis system.
Oyrenophora tritici-repentis causes tan spot of wheat on durum and common wheat as well as numerous other grass species.
Races of P.tritici-repentis are determined by the presence or absence of three host-specific toxins. Each compatible interaction between a basic race and its corresponding susceptible host differential line was found to be mediated by a different host specific toxin.
How could a mutation from avirulence to virulence in a pathogen lead to a decrease in pathogen fitness?
If Avr-encoded proteins perform some other useful, and perhaps vital, cellular function in the pathogen, the loss or mutation of the avirulence allele may compromise the fitness of the organism.
Why would a pathogen avirulence gene have higher levels of diversity than other pathogen genes?
