Quantitative and non-host resistance in pathogen-plant interactions Flashcards
What are the key properties that differentiate quantitative resistance from major gene resistance? Describe at least 6 of these properties.
Major Gene resitance:
Simple inheritance
Genotype x Environment interactions rare
Hypersensitive response
No symptoms or small flecks
no epidemic
Usually detected in seedlings
Quantitative resistance:
Quantitative inheritance
G x E interactions common
Various, largely unknown modes of action
visible disease
Slow epidemic development
Often detected in adult plants
Describe how QTLs are identified. What is a LOD score?
Conceptual basis of QTL mapping is a F2 population. DNA markers throughout the entire genome are tested for the likelihood they are associated with a QTL.
For each marker locus the individual are divided into classes according to their marker genotype and mean and variance parameters for the classes are compared with one another. A significant difference in phenotype between classes at a particular locus indicates a QTL is probably nearby.
The association is mapped to descrete regions (intervals) on a chromosome, representing the space between adjacent molecular markers. This inteval is called a QTL and can be assigned a statistical probability called an LOD score.
LOD: Logarithm of the odds
A LOD score of three or more is generally taken to indicate that two gene loci are close to each other on the chromosome or that there is an association between the marker and the phenotype
Describe five major findings that have emerged from analysis of QTLs involved in disease resistance. What do these findings tell us about the likely functions of genes involved in quantitative resistance?
- A relatively small number of chromosome segments can be responsible for QR, suggesting that perhaps only a few genes are involved with QR in many cases.
- Many QRLs show race specificity, others show no race specificity
- Some QRLs have major effects, some have minor effects
- Some QRLs map to positions shared by known plant defense genes
- Some QRLs map to positions of known Major R-genes or R-gene clusters
What was the first cloned QR gene? What does it encode? How is it thought to function?
The first QRL (Lr34) was cloned and characterized by beat Keller in 2009. Lr34 provides quantitative, adult plant resistance to leaf rust, as well as yellow rust and powdery mildew.
Lr34 is associated with reduced intercellular hyphal growth, but not hypersensitivity or papilla formation. Lr34 is an ABC transporter with some similarity to PEN3, which is thought to translocate toxic compounds made in plant cell into the apoplast. Lr34 might have the same function (currently researching)
Can quantitative resistance lose its effectiveness or is is always durable? Why is it more difficult to detect a loss in the effectiveness of quantitative resistance than a loss in major gene resistance?
It is assumed to be durable, apart from two examples no one has reported on the loss of effectiveness of QR. Some other examples are recently emerging of “erosion” of QR.
if selection operates differently on the pathogen population, the evolution in the pathogen may be slower and it may take longer for the pathogen to adapt. or perhaps the pathogen is already adapting to QR but we aren’t well equipped to detect it
What are four costs associated with breeding for disease resistance?
Development costs of breeding effort
Germplasm screening and development
More expensive seed
Yield costs?
What are five benefits associated with planting disease resistant crops?
Higher yields
Higher quality
lower inputs
no ecological damage
simplifies disease management
best strategy for managing disease in developing countries
Explain the concept of productivity maintenance research (PMR). How does disease resistance breeding connect to PMR?
Productivity maintenance research refers to efforts aimed at sustaining and enhancing productivity of crops over time. Disease resistance breeding is a crucial component of PMR, since outbreaks can reduce crop productivity. Both have the same objective of maintaining and maximizing crop stability and productivity
Describe two examples of resistance genes that were shown to impose a yield cost.
When resistance is introduced from wild relatives of crop species, yield and quality often decrease
Mlo locus in barley is involved in resistance to powdery mildew, loss of Mlo activity confers resistance to mildew and deregulated leaf cell death, yields are 4.2% lower on average
RPM1 encodes resistance to Pseudomonas syringae strains
RPM1+ plants were consistently smaller tha rpm1 with smaller shoots, smaller numbers of seed pods and fewer seeds per seed pod. yield cost of 9% associated with having the RPM1 gene
What are three risks associated with growing resistant crop cultivars?
Breakdown in resistance
Over-reliance on resistance to protect yield gains
Activation of induced resistance causing yield loss
Toxic properties associated with resistance?
What is non-host resistance and why is it so difficult to study? What is the difference between “Type 1” and “Type 2” non-host resistance?
resistance observed when all members of a plant species exhibit resistance to all memebers of a given pathogen species. NHR is thought to compromise a variety of distinct mechanisms that may include the production of pre-formed toxins or barriers or the lack of essential metabolites or signaling molecules required by the pathogen.
multi-genic and the inactivation of any one component may not be sufficient to render a plant susceptible
Type I: the non-host pathogen is able to overcome preformed and general elicitor-induced plant defense responses such as cell wall thickening, phytoalexin accumulation, other plant secondary metabolites and papilla formation. Pathogenesis-related gene expression as a component of systemic acquired resistance (SAR) can be induced by general elicitors of the nonhost pathogen.
Type II: Non-host pathogen is able to overcome preformed and general elicitor-induced plant defense responsens probably by producing detoxifying enzymes. Specific pathogen elicitors are the recognized by plant surveillance system and this triggers plant defense leading to a hypersesitive response
Describe the experiments done to genetically characterize non-host resistance to barley powdery mildew in Arabidopsis thaliana. What is the main finding regarding non-host resistance to emerge from these experiments?
a series of mutant lines of Arabidopsis that had impaired host defenses were isolated. Two types of mutants were isolated: 1. PEN mutants, spores could penetrate cell 2. signaling mutants: salicylic acid pathway inactivated (PAD4, EDS1, SAG101)
Combined mutations in PEN3 and EDS1 compromised Non-host resistance to Blumeria graminis hordei (barley powdery mildew) and pea powdery mildew. The work showed that seberal different genes are involved on non-host resistance in Arabidopsis
Do you think that non-host resistance will eventually be useful in agricultural ecosystems? Explain your answer.
It depends on the mechanism of the non-host resistance. If the mechanism is similar to the detection system of the MGR and GFG response, the pathogen may be able to mutate the elicitor gene to evade recognition. But if the elicitor is essential for the pathogen, the virulent strain carrying the mutated elicitor may be a weaker pathogen
