W2, Flashcards
Give an example of a pest whose lifecycle or migration is highly dependant on environmental conditions.
The Australian plague locust only migrates (at dusk) when temperatures are greater than 20 °C
True or False?
The more life cycles (or reproduction) in a period of time, the higher the likelihood for damage.
Another way of asking the same thing:
The lower the generation interval of a pest, the higher the likelihood of damage.
True.
The more life cycles, the more likely an epidemic. If you get to making secondary inoculum quicker, you enter a feedback loop where you make more and more inoculum.
Explain what is the most fundamental aspect of the ‘Environment’ side of the disease triangle.
It’s the interaction between environmental conditions that is important, not just one aspect.
For example, Phytophthora infestans, which causes potato leaf blight, needs the interaction of cool and moist conditions to become a problem.
Describe some of the impacts of moisture that affect the pest or host and the extent of damage/disease.
- Dispersal of pathogens (e.g. fungal spores, nematodes)
- Activates dormant pathogens (spore germination, etc)
- Stimulates sporulation (e.g. downy mildew)
- Water stress (too little or too much) weakens the host, making it more susceptible to attack.
- e.g. Fusarium solani, dry root rot of beans
- e.g. Streptomyces scabies, common scab of potato
- Wet soils often favour reproduction and spread of zoosporic pathogens and most root rots and pathogens.
- Not only the amount of moisture (water) available, but its seasonal distribution is also important.
Describe some of the effects that wind has on the pest or host and the extent of damage/disease.
- Dispersal of pathogens (has the most impact with rain which washes spores down out of the atmosphere) and pests (able to fly further = wider distribution)
- Causes damage to hosts (wounds through which bacteria, viruses, and fungi can enter)
- Can dry out moisture films (which is a good thing - prevents infection and movement of pathogens)
Describe how the disease pyramid differs from the disease triangle
It includes the interaction of two more factors:
- Time
- Humans
Explain the difference between tolerance and resistance.
Tolerance:
The ability of the host to maintain its own growth or yield in spite of infection
- e.g. quick replacement of leaves or roots that were damaged by the pathogen
Resistance:
The ability to hinder the development of potential pathogens
- Can be constitutive (something that’s there all the time) or induced
- A genetic trait
There are 3 types of resistance to pathogens that plants have; describe them.
Non-host resistance:
- Plant remains healthy
Quantitative (polygenic) resistance:
- Some infections and symptoms possible
- Plants generally survive and produce
Monogenic (R gene) resistance:
- Plants are either resistant and remain healthy, or are susceptible and become severely diseased.
Explain the difference between passive, active, and learned resistance
Passive (CONSTITUTIVE):
- Genetic
- Just happens to be the way the plant grows, looks, smells, etc
- Prevents infection from occurring
Active (INDUCED)
- Genetic
- Relies on 2 layers of recognition
Learned (SYSTEMIC ACQUIRED RESISTANCE):
- Doesn’t rely on genotype specifically
- After the localised reaction to a pest attack, the plant develops a long-lasting, broad spectrum systemic resistance to later attacks
- Usually maintained for > 20 days in most crop plants
- Can be induced by applying salicylic acid (the hormone thought to be responsible) or a specific pathogen.
List some examples of constitutive defences
- Lignin/increased cell wall thickness
- More cellulose
- Cross-linking of the cell wall
- Callose layers
- Pectin
Explain the hypersensitive response (HR) in plants.
A genetic trait that allows the plant to initiate cell death around the infection site to prevent further penetration of the pathogen.
Works well for biotrophs, not so well (at all) for necrotrophs.
List some forms of barrier resistance.
- Papilla (callose) formation (e.g. under the penetration peg of a spore)
- Envelopment of bacteria in xylem
- Vascular occlusion (basically block the xylem with callose or lignin to prevent the spread of bacteria)
- Haustorial encasement (if they can’t access nutrients, they die)
- Lignification
Explain what Pathogenesis-related (PR) proteins are and do.
- Coded by the host plant
- Induced in response to the presence of substances associated with pathogens or insect pests
- e.g. chitinases induced in response to detecting chitin, a substance found in insect exoskeletons, not plants.
Explain the difference between systemic acquired resistance and induced systemic resistance.
Systemic acquired resistance:
- Requires a pathogen to first cause some damage
Induced systemic resistance:
- Doesn’t require a pathogen, but does require an organism, usually a soil-dwelling bacteria, to induce phloem-mobile signals to induce a defence response
How do plants recognise they’re being challenged by a pathogen?
2 layers of recognition which both rely on resistant gene expression.
1st ‘basal’ layer - pattern recognition receptors
- recognise any general pathogen molecule
- flagellin (major protein in flagella)
- chitin (insect exoskeletons and fungi cell walls)
- amalayse (in insect saliva)
- initiates defence response
immune response can be suppressed by viralence proteins (effectors) produced by the pathogen; that’s its way of making the plant susceptible.
2nd ‘Guard hypothesis’ layer
- ‘Guard’ (resistance (R)) proteins basically watch for any changes to the host protein caused by virulence proteins (effectors)
- If they’re detected, an ‘effector-triggered immunity’ response is initiated.
