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Plant Resistance To Pests > Final - Pathogens > Flashcards

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
Q

Why is purely asexual reproduction a bad long term strategy

A
  1. most mutations are bad

2. Once fitness is lost, you can’t get it back

26
Q

How do asexual pathogens overcome drawbacks of their asexual nature.

A

Para sexual cycle

27
Q

What is the parasexual cycle

A

Two hyphae join, and their respective nuclei fuse, mitosis crossing over occurs, and then the nuclei become haploid again with new alleles.

28
Q

Advantage of mitotic crossing over

A

Allows multiple virulence alleles to be put together from two asexual pathogens.

29
Q

Plasmid

A

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
Q

Genomic island

A

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
Q

Durable resistance -def

A

is that which “remains effective during
prolonged and widespread use in environments favorable
to the pathogen or disease spread”

32
Q

Costs of resistance gene breakdown

A

– 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
Q

Why are R genes against viruses more durable than bacteria or fungus

A

Viruses have very some genomes and can’t lose many effectors, so sometimes R-genes can be durable

34
Q

Why is PAMP triggered immunity durable, what are the draw backs

A

Broad spectrum defenses that are always on at a higher level.
Weaker/less effective than ETI triggered immunity
Comes with a fitness cost

35
Q

Gene Pyramiding

def

A

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
Q

Gene Pyramiding

advantages

A

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
Q

Gene Pyramiding

disadvantages

A

– If resistance is overcome, you may have lost all your best R genes.

38
Q

Genotype mixtures -strategy for R gene deployment

A

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
Q

Genotype mixtures -strategy for R gene deployment

-pros/cons

A

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
Q

Rotations of R gene deployment in space and time - -strategy for R gene deployment

A

– 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
Q

Vertical vs horizontal resistance durability

A

Horizontal is durable, vertical is not.

Horizontal is non-race specific

42
Q

Steps in QTL analysis:

A

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
Q

Tolerance- strategy for durable resistance

A

tolerance doesn’t exert selection pressure

44
Q

QTL mapping advantages over classic genetics

A

of genes involved in a trait, location, GxE effect

Plant Resistance To Pests (6 decks)

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