Plant resistance to arthropods. Flashcards

Content for final exam.

1
Q

4 Types of plant traits.

A

Biochemical, morphological, physicochemical, and physiological.

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2
Q

What is phenotypic plasticity?

A

The ability of one genotype to produce more than one phenotype when exposed to different environments. A plant’s resistance phenotype depends on its its history of interactions with biotic and abiotic factors in the environment.

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3
Q

Differences between HPR and IPI literature.

A

HPR is concerned primarily with intraspecific variations in resistance (among plant varieties). In contrast, IPI literature deals with variation in resistance at several levels: within and among various plants and insect populations, intraspecific variation, and interspecific variation.

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4
Q

What is digestion?

A

Enzymatic and non-enzymatic degradation of chemical polymers to smaller molecules that can be absorbed through the midgut epithelium.

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5
Q

Describe gene-for-gene interactions.

A

Single plant genes encode important regulatory elements in some plant-insect systems, and activation of these genes result in a cascade of changes that result in resistance. This type of phenomenon usually involves a type of resistance called “vertical resistance”.

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6
Q

Successful examples of HPR as a primary means of pest control.

A

Grape cultivars to grape phyloxera
Wheat to Hessian fly
Rice to brown plant hopper

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7
Q

What is plant resistance?

A

Any plant trait that influences any aspect of the interaction between the plant and herbivore is potentially a basis (cause) of resistance. Different genotypes typically differ in one or more traits that can influence a plant-herbivore interaction. Therefore, plant resistance is the composite effect of all heritable plant traits that reduce the impact of potential herbivores by altering some aspect of the interaction between a plant, an herbivorous, and the natural enemies of the insect. The ultimate effect is the increased plant yield or fitness.

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8
Q

Antibiosis, antixenosis, and tolerance definition.

A

Antibiosis: plant traits that negatively affect the fitness (growth, development, fecundity) of pest insects.

Antixenosis: comprises those plant traits that negatively affect the behavior of pest insects, resulting in (generally) reduced colonization of resistant plant.

Tolerance: comprises those plant traits that allow a plant to recover from/compensate for injury, thereby reducing damage per unit injury.

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9
Q

How are the three types of resistance distinguished experimentally?

A

Antibiosis – no choice experiments. Antixenosis – choice experiments. Experimental demonstrations of tolerance are more difficult than experimental demonstrations of other types of resistance. Tolerance can be quantified in at least three ways.

I – Genotype (susceptible vs resistant) selection for endpoint (usually yield or seed production, mortality) comparison .Treatment groups with different levels of injury are established to compare the effects of injury with respect to the endpoint in different genotypes.

II – Injury response curves. Density curves are a common example in which the x-axis is some measure of injury and the y-axis is some measure of fitness or yield.

III – Analysis of covariance in which the slopes of the relationships between injury and fitness are compared among genotypes. Significant differences in slope indicate genotypic differences in tolerance.

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10
Q

Where does digestion take place? Role of peritrophic membrane?

A

The alimentary canal of insects is divided into three regions: foregut, midgut, and hindgut. Midgut, which is the primary site of digestion, contains the ventriculus (stomach), gastric caecae , and endo/ectoperitrophic spaces. Enzyme secretion, digestion, fluid secretion and nutrient absorption take place in the midgut. The main role of the peritrophic membrane is to separate the gut into ecto and endo peritrophic spaces. The peritophic membrane is porous, which may allow partially digested proteins through while excluding undigested proteins. Thus, the peritrophic membrane may allow compartmentalization of digestion and digestive enzymes.

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11
Q

Manifestations of post-ingestive resistance. Discuss the effects of post-ingestion on herbivores that are not adapted to resistance-related traits.

A

These effects can range from acute toxicity that results in high mortality to relatively small changes in developmental time or insect growth. These effects are categorized as antobiosis effects, but might have very different implications for pest management.

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12
Q

General considerations:

Resistant plants/secondary metabolites and other resistance-related traits have negative effects on herbivorous insects.

A

a) These effects are specific-specific, the same chemical may have dramatic effects on one insect but no effect on another (adapated/specialist) insect.
b) Structurally similar compounds may have divergent effect on the same insect.
c) Toxic chemicals often, but not always, have deterrent effects. Experiments often do not disentangle deterrency from toxicity. How can we disentangle these two effects?
d) On most studies on the effects of secondary metabolites on insects, the effects are assessed at the whole-insect level of analysis. The mechanisms by which secondary chemicals bring about their whole-organisms effects are often not known.
e) The negative effect of secondary chemicals can be manifested in numerous ways, determined in part by the experimental methods used.
f) A distinction can be made between compounds that interfere with digestive processes in insect guts. (i.e., never enter the body of the insect proper; the target site is in the gut) and those that pass through the epithelium and interact with a target site in the insect. The former may be called anti-nutritive compounds or digestibility reducers; the latter, toxins.

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13
Q

3 categories of resistant-related traits mode of actions and specific examples of each: toxin vs antinutritive vc antidigestive.

A

Anti-nutritive compounds or digestibility reducers interfere with digestive processes in insect guts. (i.e., never enter the body of the insect proper; the target site is in the gut. Toxins pass through the epithelium and interact with a target site in the insect.

Toxin: Tomatine – tomatine destroys membranes by interacting with cholesterol.
Canavanine – Canavanine absorbed into hemolymph, gets incorporated into tissues.
Hydrogene cyanide and glucosinolate.

Anti-nutritive compounds: polyphenol oxidase and other oxidative enzymes. Highly reactive oxidized phenolics interact with proteins and render them less nutritious. Result is less proteins
digested and absorbed.

Anti-digestive compounds: proteinase inhibitors. Reduction in amount of protein digested = anti-digestive.

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14
Q

What are some of the “drivers” of phenotypic plasticity?

A

Water stress; biotic factors such as prior herbivory, plant density, and predator/parasitoid behavior; nutrient availability.

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15
Q

Types of induced resistance.

A
Hypersensitive response
 Direct induced resistance
 Indirect induced resistance
 Plant stress-induced responses
 Interplant communication
 Priming
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16
Q

Types of induced resistance. Describe Hypersensitive response.

A

The resistance of some plants to some pathogenic microorganisms involve the induction of a rapid and localized programmed cell death response at the site of attempted infection. This programmed cell death is called hypersensitive response and is governed by specific resistance genes in the plant that recognize the presence of products of corresponding avirulence genes in the pathogen in a so called gene-for-gene interaction.

17
Q

Types of induced resistance. Describe Direct induced resistance.

A

Refers to a phenomenon in which rapid changes in plant biochemistry, physiology, or morphology directly reduce the quality of the plant as a host for subsequent herbivores. Representatives of all major classes of secondary chemicals have been shown to be inducible, and the levels of many types of primary chemicals are affected by herbivory as well.

18
Q

Types of induced resistance. Describe indirect induced resistance.

A

Other changes induced in plants by herbivory do not affect subsequent herbivores directly, but rather affect them indirectly by enhancing the effectiveness of carnivorous natural enemies of the herbivore.The best-suited form of indirect induced resistance involves the release by damaged plants of volatile organic compounds that attract predators and parasitoids of the herbivore.

19
Q

Types of induced resistance. Describe Interplant communication.

A

The idea that damaged plants may emit signals that induce resistance in neighboring, undamaged plants.

20
Q

Steps in an induced response.

A
Recognition phase(danger perception)
	- Injury/production of elicitors and effectors
	- Reception by plant
Signal transduction
	- Local signaling
	- Phytohormonal signals 
Plant response
	- Changes in gene expression
	- Production of resistance-related traits
Interaction with subsequent attacker
21
Q

Examples of incompatibility between plant resistance and biological control.

A

Resistant varieties, by reducing the number of pests (prey), can lower prey:preadator ratios such that predators are more effective. Use of resistant varieties can result in increased herbivore movement or reduced herbivore growth rates, both of which can benefit predators/parasitoids. Smaller herbivores may be better prey. Increase of greenbugs in the presence and absence of parasites caged on greenbug-resistant. There was a great reduction in performance of greenbugs caged in resistant barley varieties due to the presence of parasites.

22
Q

Distinguish polygenic vs monogenic resistance.

A

Polygenic resistance: Multiple phenotypic traits are involved in resistance, and multiple genes involved in determining levels of each of these phenotypic traits.

• Variation is continuous/quantitative rather than discrete/qualitative
•Resistance often present at low frequencies in germplasm (may need to screen thousands of
lines, special methods sometimes needed)
•High levels of resistance often not present or present only in unimproved germplasm
•Phenotyping is difficult: Level of resistance expression is environment-dependent; insect
populations variable
•Resistance may entail costs (yield drag)

Monogenic resistance: A single resistance-related trait might have a large effect on resistance, and levels of this trait might be controlled by one or a few genes.

  • Discrete, qualitative differences in resistance; often, high level of resistance
  • Phenotyping is more straightforward
  • Rarer than polygenic resistance, but some examples are well-known
  • Gene-for-gene interactions
  • Not as context (environment)-dependent
  • Resistance costly (yield drag)
23
Q

Effector x elicitors.

A

The plant basal immune system can detect broadly present microbe-associated molecular patterns (MAMPs, also called PAMPs) and induce defenses, but adapted microbes express a suite of effector proteins that often act to suppress these defenses. Plants have evolved other receptors (R proteins) that detect these pathogen effectors and activate strong defenses. Pathogens can subsequently alter or delete their recognized effectors to avoid defense elicitation, at risk of a fitness cost associated with loss of those effectors.

24
Q

Examples of gene-for-gene interactions.

A

Waring et al (2003). Apple/Ctenospseustis. Cross of liberty (ss) x Prima (rs). Susceptible insects showed no survival to pupation.

25
Q

Preference performance hypothesis.

A

Natural selection will favor oviposition preference for host plants on which offspring perform best, revealing a positive correlation (genetic or phenotypic) between oviposition preference and offspring performance. On the other hand, some herbivorous insects show a poor correspondence between oviposition preference and offspring performance. The weak preference–performance correlation may result from oviposition on to introduced host plants or a relative shortage of suitable plants or plant parts.

26
Q

Enemy-free space hypothesis.

A

Natural selection for utilization of host plants may be partly determined by enemy-free space. The enemy-free space hypothesis predicts that variability in the relative safety of alternative niches will influence the evolution of herbivore niche preferences. The cage experiment supports the enemy-free space hypothesis, because the preference of P. versicolora for S. sachalinensis has been favored by the relative safety of S. sachalinensis com- pared to S. miyabeana.

27
Q

Slow growth high mortality hypothesis

A

The slow growth/high mortality hypothesis predicts that herbivorous insects feeding on suboptimal host plants are subjected to higher predation mortality owing to the longer time spent in the vulnerable juvenile stages compared with conspecifics feeding on optimal plants. Larvae raised on S. viminalis developed faster, grew larger and survived better than those raised on S. dasyclados (unsuitable willow species).

28
Q

Advantages and disadvantages of HPR as a management tatic.

A

Advantages:

  • Low cost to growers
  • Integratable in theory with other tactics
  • Benefits accrue over space and time (area-wide), sometimes sustainable
  • Simple to use if primary strategy

Disadvantages:

  • Long and difficult process to develop; requires considerable infrastructure
  • Incompatibilities
  • Difficult to use low levels of resistance optimally
  • Some forms unstable, not sustainable
29
Q

Painter’s “steps in applied hpr program” – what is involved in screening of genotypes?

A
Pest biology
	“Screening”
	“Mechanistic” studies (categorization of resistance)
	 Breeding
	 Implementation

Screening: Evaluation of plant genotypes for resistance. Goal: To characterize plant genotypic variation in resistance to an arthropod pest in order to:
1) identify resistant genotypes that can be used immediately in an IPM program OR
2) identify resistant genotypes that can be used as donors in a breeding program
Usually intraspecific variation in resistance is of greatest interest.

30
Q

How are screening experiments conducted?

A

Precise methods used depend on biology of crop-pest interaction

Expose all or parts of plants of genotypes of interest to uniform populations of pests, measure appropriate endpoint – injury, insect performance, insect abundance, etc.

  • Details will vary depending on crop, pest biology, type of injury, putative mechanism of resistance
  • Often choice experiments (no-choice experiments may come later)
  • Plant resistance is usually a relative phenotypic trait, so susceptible and/or resistant standards needed
  • Screening for tolerance requires special methods
31
Q

Direct vs indirect resistance. Examples

A

Direct defense: Plant defense is the result of complex interactions among multiple “toxins”, “antinutritive/antidigestive” compounds, and “nutrients”

Indirect defense: Plant traits facilitate the activities of natural enemies of the herbviore
• Most common example: plant produces volatiles following attack by herbivores, and these volatiles
attract natural enemies
• Also, plants produce extrafloral nectaries following attack, and these help attract and retain naturalenemies
• Resistance-related traits can interfere with natural Enemies
• Slow growth of insects on resistant plants increases the success of natural enemies

32
Q

What types of experimental approaches can be used to determine whether a resistance-related trait is contributing to/ causing plant resistance?

A

Manipulative (Removing trichomes improves larval performance)
- transgenic approaches
- plant mutants
Approaches to elucidate causal roles of resistance-related traits
- Artificial diet studies
- Correlative studies
Use of different varieties with different levels of trait