Final - Pathogens Flashcards

1
Q

Protein Mediated Resistance results in

Strategy for pathogen-derived resistance to viruses

A

Coat protein mediated resistance.
-interferes with virus reassembly via over expression of proteins
-
Results in moderate and highly variable levels of resistance (delay in symptoms, decreased virus concentrations)

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2
Q

RNA Mediated Resistance results in

Strategy for pathogen-derived resistance to viruses

A

-RNA silencing (most common natural form of plant resistance to viruses)
Often results in complete immunity but displays a high level of sequence specificity

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3
Q

Risks associated with transgenic virus resistance

A
  • Pollen flow: genes moving to wild relatives
  • Interfere with or stop the plant’s natural gene silencing mechanisms
  • Non-target effects: Bt and monarch butterflies
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4
Q

Transgenic strategies for fungal and bacterial disease resistance

A
  • Intro of R-genes from unrelated plant species
  • Detoxification of necrotrophic virulence factors (toxins, cell wall degrading enzymes)
  • Over-expression of pathogensis related (PR) proteins
  • Activation of signalling pathways
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5
Q

R Gene Transfer- why it could work

A
  • plants have 100s of R-gene sequences
  • Thousands of non-ag plants are potential donors
  • R-genes are efficient, only activate defenses when needed
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6
Q

R Gene Transfer- potential problems

A

-Not very durable because R-genes lead to further selection within the pathogen. Often, by the time a new cultivar is released the pathogen already has resistance to that R gene

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7
Q

For more durable resistance we need more R genes because

A

Once a plant is able to recognize an effector, the pathogen changes effectors and is virulent again. Need a new R gene to recognize the new effector

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8
Q

Example of transfer broad spectrum resistance

A

Transferred a gene from Arabidopsis that keeps basal defense on at a higher level into susceptible tomato plant to make a resistant tomato plant.

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9
Q

PR protein function

A

Commonly enzymes that attack fungal cell walls

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10
Q

Potential issues with Over-expression of PR proteins as a defense strategy

A

Stressful on the plant and takes a lot of energy. You don’t get high levels of resistance either, so it’s not really worth the cost.

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11
Q

How to exploit RNA silencing

A
  1. Find the gene to be silenced
  2. transform it in two orientations
  3. It will be expressed as double stranded RNA (harpin shaped)
  4. Signals enzymes in the cell to cut it up into siRNAs (small interfering RNAs)
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12
Q

Two major Evolutionary forces driving coevolution in the gene for gene system

A

Directional selection: Favoring greater host resistance and pathogen virulence (arms race)
Balancing: Selection favoring rare alleles or different genotypes in different environments

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13
Q

Polymorphisms can be maintained in a gene-for-gene system by:

A
  1. cost of virulence (losing an effector)
  2. Cost of resistance (plants cost)
  3. Multiple alleles at a single locus keeps resistance broad bc only 2 R genes are passed at once
  4. Limited spread between local populations = less mixing in the meta population
  5. Multilocus inhertiance - if we have 20 genes involved in an effect, can have some variation and still get the same effect
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14
Q

Evolutionary forces of pathogen resistance

A
  1. Mutation
  2. Genetic drift (a loss of genetic diversity)
  3. Gene Flow
  4. Reproductive systems
  5. Selection
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15
Q

Mutations

A

the ultimate source of genetic variation (new alleles)

A large population will generate more mutations than a small one

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16
Q

Mutation- Selection Balance

A

Frequency of virulent allele at equilibrium

fe = u/s

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17
Q

P

A

Frequency of dominant allele (virulence)

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18
Q

q

A

Frequency of recessive allele

19
Q

Gene Flow
-what
how to capitalize on it

A

Exchange of alleles between geographically isolated populations of asexual reproducing pathogens. (between races, wheat stem rust from mexico could deploy multiple R genes south to north)

20
Q

Sexual reproducing pathogens have lots of diversity because of

A

recombination

21
Q

Pros/Cons of out-crossing (sexual reproduction)

A
  • Potential for rapid adaptatation in changing environment

- bad- frequent recombination tends to break up co-adapted combination of alleles.

22
Q

Asexual/inbreeding pros/cons

A
  • Potential to retain co-adapted combinations of alleles through time
  • bad- limited adaptation to to new environment (or an R-gene)
23
Q

Mixed sexual reproduction def, advantage

A
  • A sexual cycle, with lots of asexual cycles. Allows better retention of adapted genotypes with ability to bring in new alleles
  • most pathogens have this
24
Q

Why does it take asexual pathogens longer to develop r virulence to multiple genes

A

It takes time for all the virulence genes to join together because it happens via mutations.

25
Why is purely asexual reproduction a bad long term strategy
1. most mutations are bad | 2. Once fitness is lost, you can't get it back
26
How do asexual pathogens overcome drawbacks of their asexual nature.
Para sexual cycle
27
What is the parasexual cycle
Two hyphae join, and their respective nuclei fuse, mitosis crossing over occurs, and then the nuclei become haploid again with new alleles.
28
Advantage of mitotic crossing over
Allows multiple virulence alleles to be put together from two asexual pathogens.
29
Plasmid
All bacteria have plasmids which are an extra chromosonal section that will duplicate itself and occasionally be incorporated into the genome, or it can be exchanged with other bacteria via phages into their genomes.
30
Genomic island
Occurs when genes get grouped together because of their effect on fitness. Can get virulence to as many R genes as you can imagine. How bacterial resistance works
31
Durable resistance -def
is that which “remains effective during prolonged and widespread use in environments favorable to the pathogen or disease spread”
32
Costs of resistance gene breakdown
– Cultivars need to be replaced – New R genes are then needed and the supply of R genes is not infinite – Cultivars take time and money to develop – Epidemics can occur after breakdown
33
Why are R genes against viruses more durable than bacteria or fungus
Viruses have very some genomes and can't lose many effectors, so sometimes R-genes can be durable
34
Why is PAMP triggered immunity durable, what are the draw backs
Broad spectrum defenses that are always on at a higher level. Weaker/less effective than ETI triggered immunity Comes with a fitness cost
35
Gene Pyramiding | def
Simultaneous deployment of several R genes in the same cultivar. Ideally, R genes should be undefeated at the time of deployment. If a new gene is simply added to series of already defeated R genes, it is not really a pyramid.
36
Gene Pyramiding | advantages
Pathogen has to mutate at multiple Avr loci simultaneously, which should be very rare if the Avr loci are independent. – Crops are highly resistant until breakdown. – Crop is as uniform as other pure-lines or hybrids.
37
Gene Pyramiding | disadvantages
– If resistance is overcome, you may have lost all your best R genes.
38
Genotype mixtures -strategy for R gene deployment
several R genes, but in different plants. – Reduces density of plants susceptible to any pathogen component. – Resistant plants intercept inoculum. – Resistant reactions may induce some systemic resistance.
39
Genotype mixtures -strategy for R gene deployment | -pros/cons
pro=**Reducing selection pressure on the pathogen for virulence** concern= Concern is the development of complex races (bigger problem with pathogens that have a sexual cycle) Resistance to multiple R genes
40
Rotations of R gene deployment in space and time - -strategy for R gene deployment
– Each R gene is deployed over a limited number of years or area and is withdrawn before the Avr gene becomes frequent. – Disrupts the directional selection for virulence on a single R gene. drawback= – Requires development and increase of many cultivars.
41
Vertical vs horizontal resistance durability
Horizontal is durable, vertical is not. | Horizontal is non-race specific
42
Steps in QTL analysis:
1) Make a large segregating population that is segregating for the trait of interest. 1) Evaluate and score the individuals (or lines) in the population for the trait. 1) Score the individuals for DNA markers spread throughout the genome. 1) Perform statistical tests for associations between the markers and the trait.
43
Tolerance- strategy for durable resistance
tolerance doesn't exert selection pressure
44
QTL mapping advantages over classic genetics
of genes involved in a trait, location, GxE effect