Summary Breeding for stress tolerance and quality
Resistance to biotic stress
Steps towards a breeding strategy:
1. What is the breeding goal?
2. Where to find genetic variation?
3. How to test parents and progeny for the desired traits?
4. What is the target region?
5. Which development stage or generation to test?
6. How to develop a new variety? Preservation of agriculture
Resistance against biotic stresses pathogens and pests
Primary consumers
Herbivores Large, mobile, cause biting Rabbits, caterpillars, snails
damage, food plants
Parasites Rather immobile, sucking, Orobanche, striga, aphids, white
visible organism, host plants fly, nematodes, scale insects
Pathogens Immobile, MO, in or on the Fungi, oomycte, bacteria,
plants, may cause symptoms, mycoplasms, viruses
host plant
Defence strategies:
Avoidance: prevents intimate contact. Done by camouflage, mimicry, thorns, hairs, smell, colour, taste
and cleistogamy
Resistance: restricts infection (growth, development,reproduction) after intimate contact. Physiological,
mechanical, active or passive. Regarding the amount of MO present in the plant.
Tolerance: restricts damage due to the infection. True tolerance vs ability to recover. Yield loss per
amount of parasite, in comparison with disease free crop.
Disease: physiological disturbance of a plant or of a substantial part of a plant, caused by a biotic stress
factor or a combination of stress factors, resulting in symptoms. Or; physiological disturbance by abiotic
factors, like toxic compounds or nutrient deficiency.
The plant innate immune system is the zig-zag model
PAMP recognition triggers immunity resistance
TTSS effectors suppress immunity susceptibility
R proteins recognize effector activities resistance
,General defense: the mechanism by which a plant species defends itself against the large majority pf all
potential attackers. Consists out of preformed barriers (wax layers, rigid cell walls, anti-microbial
enzymes, secondary metabolites)
Inducible defense: general elicitors or PAMPS trigger PAMP triggered immunity
Basic-compatibility: pathogen delivered effectors silence the general defence
Pathogen specific resistance/immunity: Avr/R genes. At least one effector is recognized in some cultivars
to elicit resistance
Plant Pathogen Interaction
General morphology & Genes for parasitic life e.g. penetration of stomata
physiology processes
General defence factors Pathogenicity negating “general Basic compatibility
defence”
Pathogen specific defence Certain avirulence genes Race-cultivar specific resistance
Nonhost resistance: resistance shown by an entire plant species to all genetic variants of a pathogen.
Plants are non-host for the majority of potential pathogens. A plant species is a non-host to a potential
pathogen species, if no individual of the plant species is known to allow any member of the potential
pathogen species to successfully reproduce. Complete and durable type of resistance. Acts at a species
level. Diversified mechanisms, e.g. echanisms contributing to broad resistance, the formation of papillae
and cell death like HR. hardly used in breeding programs.
Crops can be turned into non-host for their pathogens by:
- Use of genes for non-host resistance
- Use of PTI components
- Stack of R-genes
- Silencing of S-genes
Pathogenomics: finding the effectors of a pathogen. The effector can be used to find a R gene.
Plant S-genes: plant genes that are required for susceptibility to certain pathogens. Genetically, S-genes
can be defined as dominant genes whose impairment leads to recessive resistance. Categories:
- Effector targets,
- negative regulator of plant defense
- Susceptibility factors
- genes improving pathogen establishment
- genes interfering with plant defense response
- genes involved in feeding the pathogen.
S-genes are orthologues across plant species, and function of S-genes are conserved for many pathogens
Broad defense mechanisms are identifiable and effective to a wide range of potential consumer species.
They contribute to non-host status of plant species. E.g. presence of anti-microbial compounds (α -
tomatin in tomato = passive, or HCN in bird’s-foot trefoil = active). Adaptation by consumer:
- breakdown of anti-microbial compound
- tolerance of anti-microbial compound
- utilization of anti-microbial compound
- prevent/suppress induction of anti-microbial compound
variation in host range
polyphagous consumers are generalists
monophagous consumers are specialists
in between oligophagous consumers
,Forma speciales: unit within the consumer species that is distinguished by its host range. Levels of
speciation between formae speciales varies in crossablility, electrophoresis patterns(DNA sequence) and
morphology.
Host resistance: resistance after intimate contact after haustorium formation. Hypersensitivity is post-
haustorial and can occur earlier or later in the infection process
Race specific resistance = vertical resistance.
Race-non-specific resistance = horizontal resistance
Physiological race = Race, also called “pathotype”. In insects: biotype, in viruses: strain
Definition: unit within (fungal) species or within forma specialis charactersied by virulence spectrum on
cultivar range of host species.
Isolate: collected and maintained sample of the parasite.
Gene-for-gene interaction: a gene for resistance is only effective when the infecting parasite carries the
corresponding gene for avirulence
- interaction means incompatible plant/pathogen combination. Plant is resistant and pathogen avirulent
+ interaction means compatible plant/pathogen combination. Plant is susceptible and pathogen is
virulent’
Differential interaction: phenomenon whereby the ranking in susceptibility of two plant genotypees
depends on the genotypes of the pathogen isolates to which they are exposed. There is a clear cultivar x
race interaction.
Genetics of hypersensitivity resistance
- there are often many R-genes available, at different loci
- each R-gene corresponds with different Avr, and therefore in principle has different reaction
pattern to collection of isolates
- per plant genotype usually only 0,1, or 2 R-alleles the other loci are r
- each locus is often cluster of functional and nonfunctional homologues, with different alleles
- R-genes are not expressed in all tissues or all developmental stages
- R-genes can be hidden by suppressors (in recognition, signal transduction and defense
responses)
expression of resistance may also depend on:
- plant parts
- development stage
- environmental factors
how to find genes required for R-genes
- wild cultivars with resistance
- mutagenesis find susceptible one, study wat is mutated
how to find out if 2 cultivars carry the same resistance gene?
- Cross the 2 cultivars self 1 analyze f2. If different genes 1:15 segregation. If same gene, 1:3
segregation for susceptibility.
- Note that R-genes can be linked aswell
Differential series of cultivars: a collection of cultivars that discriminate maximally between the possible
races of the pathogen.
- Series on the basis of experience
- Series of cultivars with known genes for resistance
- NILs carrying the known genes for resistance in the same background
, Purpose of differential series: determination of Avr/avr factors occurring in pathogen isolates (= their
race identity). To carry out virulence surveys
Amount of races that can be discerned maximally by a differential set of cultivars consisting of N
genotypes is N2
Durability: a resistance is durable if It remains effective despite a wide spread application in cultivars,
grown over large acreage for a long time in an environment suitable for the pathogen
Factors that affect the evolution of populations of plant pathogens
- Mutations
- Reproduction/mating system
- Gene flow
- Population size
- Selection
Partial resistance: resistance that leads to reduced infection, despite a compatible (non HR) infection
type
AUPDC: area under disease progress curve
Latency period of rust fungi is the time that elapses between germination of the spore and maturation of
the resulting uredium ‘pustule’. Since there are many uredia on the leaf, we determine the latency
period as the time between start of the dark-humidity period and the maturation of 50% of the final
number of resulting pustules. Says something about the generation time of a pathogen. Relative
infection frequency and relative spore production about reproduction factor
LP50= A + (B/C) * D
A: time from inoculation until last counting before 50% of pustules were mature
B: time between last counting and first counting after 50% of pustules were mature
C: increase in number of pustules during period B
D: 50% count minus number of pustules at the start of period B
Mechanisms of partial resistance:
Pre-haustorial papilla formation, low infection frequency, long latency period
Research questions:
- How many QTLs?
- How large is their effect?
- Do they affect all components of PR?
- Are QTLs consistently detected?
- Are QTLs isolate-non-specific?
Partial resistance often inherits quantitatively
Difference partial resistance and tolerance
Tolerance need damage + amount of pathogen
Partial resistance can lead to tolerance, can lead to sensitivity, depending on damage
A pathogen has species level formea speciale
A pathogen has cultivar level specific isolate
The way towards a resistant cultivar:
1. Should we induce resistance?
2. Where to find resistance? 3. Where to test the parents?
