Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

plant biology 3 > disease > Flashcards

disease Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Biology flashcards Biology 101 flashcards
1
Q

what is plant pathology?
why does it exist?
which trade offs exist

A

the study of plant disease
it exists because to control plant diseases they must be understood
economic costs, effectiveness and environmental imapcts all exist (trade offs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

define plant disease and list its causes

A 
when a causal agent (apthogen) causes continuous irritation or injury or abnormality 
biotic causes (microbes)
abioic causes (drought, salt stress etc)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

name 4 examples of plant disease

A

1840s: potato light blight cuased potato famine in Ireland
1870s: Srilanka outbreak of Coffee rust devestated the economy. transtition from coffee to tea
1940s: in bengal brown spot disease of rice occured causign famine
since 1970s: southern corn leaf blight of Maize has caused $1BN damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

discuss details of the Irish potato famine (time, causual agent, causes, effects, why effects were severe)

A

Time: 1940s
causal agent: Phytophthora infestans (oomycete: fungus like)
effects: 500,000 died, 1 million emigrated
why effects were bad:
-unknown cause
-favourable weather conditions
-reliance on potatoes
-lack of government response or control mechanism
-polycyclic life cycle; quick build up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

state different biotic pathogens

A 
viroids: pieces of RNA which alter expression
viruses
bacteria
fungi
plants; nutrient stealing witchweed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

whats the difference between a pathogens life cycle and infection cycle

A

life cycle is birth to death

infection cycle is infection to spread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

decribe pathogen infection cycles

A

infection; spore lands on leaf and germinates and grwos into the leaf
growth
reproduction
spread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

describe the P. infestans life cycle

what has synthetic modelling taught us about the life cycle

A

1) Fungus overwinters in plant tubers
2) During spring, the fungus grows and produces sporangia which are structures containing spores; wind dispersal of sporangia occurs to leaves of other plants
3) sporangia either
- –germinate direction as germ tubes (hyphae into plants)
- –germinate indirectly as 6-8 zoospores which then form cysts (fluid sacs) which germinate as a germ tube hypha and infect the leaf.
4) once grown in plant, sporangia are produced which drop to the ground and and spread the disease further

direct germination occurs at temperatures above 18 degrees
indirect germination occurs at temperatures below 18 degrees

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what different mechanisms do pathgoens use to get nutrients from plants

A

biotrophs: keep plant alive and gain nutrients
necrotrophs: kill plant and gain nutrition from dead tissie
hemibiotrophs: initially keep plant alive but eventually kill it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

is P. infestans biotrophic, necrotrophic or hemibiotrophic

A

hemibiotrophic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

whats the difference between disease signs and symptoms

A

signs: pathogen structures observed
symptoms: reactions occuring: cell death, yellowing, abnormal shape, stunted growth etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why is disease management difficult

A

trade offs
resistance emerges
plants used change
environment change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

list ways of controllign plant disease

A 
regulations to stop spread
changing cultural practises
resistant plants
biological control
chemical control
integrated approach
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

current state for pathogen control

A

lots of chemical control being used; policies to reduce usage are being implimented
biological cotnrol has little role; remains potential area and use is slightly increasing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

define endemic, epidemic and epidemiology

A

endemic; disease present at low levels

epidemic: disease present in high percentage of population
- could be small populaiton like a field
- could be low level damage
epidemiology: studying disease development so that diseases can be managed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the 3 requirements for an epidemic

A

virulent pathogen present
sufficient inoculum at the correct time of the season
favourable environmental conditions for pathogens life cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the two pathogen life cycles

A

monocyclic: pathgoenic cycle occurs once per growing season
polygenic: pathgoenic cycle occurs mor than once per growing season; disease can build up to high levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the logistic equation used to describe

A

polycyclic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

discuss logistic growth of polycyclic diseases (define x and r)

A 
x= the percentage of leaf area infected
r= the basic infection rate (days). the larger the r the quicker the disease builds up
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

describe monocyclic diseases

A

one infection cycle oer growing season
gradual build up of inoculum in a logistic way
smut disease: pathogen produces spores when the plant flowers (once a year)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

describe environmental effects on disease

A

chemical: soil pH and nutrients
physical: temperatures, moisture and wind
biological: other organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

describe the disease triangle

A

environment effects both host and pathogen
environment and host effect eachother
host effects environement in a very minor and localsied way (pathogen too possibly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

describe and discuss disease modelling

A

predicting how disease will build up under certain conditions
results based on computer programs can be compared to real life results in order to update model
models can be used to help direct resources such as chemical control
easier to use a model compared to investigation in real life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

discuss the two appraoches to disease modelling

A

1) empirical (meaning based on observation rather than theory); observe the amount of disease present and correlate it to the environment and amount of inoculum observed
2) theoretical: doing detailed analysis of how disease develops
a) analysis method: do an overall description than add details
b) synthesis method: understand the beahaviour of each part in order to understand the system as a whole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is synthetic modelling

A

examining the the environment effects each stage of the infection cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are the different measures of disease severity

A

-basic infection rate (r) number of cases one cases of infection one case generates on avergae over the growing season
-area under disease progress curve (AUDPC) ona time vs x graph (x meaning % leaf area infected)
-days to 50% blight (x)
final disease severity (x)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are the two types of fungicides
which is more specific
advantages and disadvantages of each

A

protectant: remains on plant surface and prevents initial infection
systemic: taken up by plant and prevents pathgoen growth (even after initial infection event)
protectant is non specific and systemic is very specific
systemic is better in lots of ways;
-no cance of toxicity to plant,
-lower spray frequency
-lower dosage needed
-lower cost
-lower environmental hazard
PROBLEM: resistance to systemic fungicides is very common compared to resistance to protectants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

describe the mode of action of both types of fungicides

A

protectant: non specific modification of protein SH groups
systemic: specific action against cellular processes, for example:
a) benzimidazoles; benomyl; bind to beta-tubulin protein and prevent microtubule formation; cell division stops
b) ergosterol biosynthesis inhibitors (EBIS); azoles; ergosterols are an important component of true fungi membranes for integrity. biosynthesis enzymes like CYP51 are inhibited
c) Acylalanines; mefanoxam; interfere with oomycete RNA synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

four ways pathogens develop resistance to chemical control

discuss one case study

A

1) detoxification; converson to harmless substance
2) overexpression of target gene
3) target site alteration by mutation;

  • those sprayed with mefenoxam showed a mutation in the RPA160 subunit of RNA POL1 which was associated with resistance (86% association)
  • transfer to sensitive strains showed resistance but slower growth; other factors at work

4) target site exclusion; making sure target site cant come into contact with the protein
a) reduced uptake of chemical
b) sequester chemical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what the three strategies against pathogenic resistance

A

1) crop management
a) use less sensitive cultivars
b) use good agricultural practises; plant crops a certain distance apart

2) use effective deployment
a) only use fungicide when needed
b) dont use fungicide to “cure plants”; pathgoen population will be very large so resistant more likely to arise
c) dont use too little fungicide
d) use models to work out the best time for deployment

3)use different/multiple fungicides at once; even if pathogens confer resistance to one fungicide, resistance to the second one simultaneously is unlikely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

discuss the case study for chemical control

explain the pattern observed

A

Using acy-lala-nines to control P. infestans causing Potato late blight

1978: metalaxyl introduction in Europe
1980: isolates become resistant so the fungicide was withdrawn.
from here onward the number of resistant isolates began decreasing
1985: reintroduction in conjunction with another fungicide (protectant)
resistance of isolates increased to 70% but then stabilised at 50%
metalaxyl is still used and remains more effective than just using the protectant alone

different strains exist, some are sensitive, some are resistant. when the fungicide is used the resistant strain becomes dominant. lack of fungicide use causes the sensitive strain to beocme dominant (less energetically expensive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are rules which prevent resistance to fungicides like mefanoxam

A

1) use early in season (small populations)
2) done use curatively
3) maximum of 3 applications
4) done use of potatoes grown from seed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

discuss how farmers use modelling

A

farmers use “desicion support systems” to help them apply fungicide in an effective way. for example if theres not much inoculum present then the program will suggest not applying fungicide at all
takes into account weather changes

34
Q

describe different types of forecasting

discuss forecasting systems for potato late blight

A

1) forecasting based on the environment (temperature, moisture etc)
a) smith period system: you are at risk if the temperatures is below 10 degrees and the RH is above 90% for more than 11 hours on 2 consecutive days
b) hutton period: (came about because smith period was not stringent enough) same parameters as smith period but for 6 hours rather than 11. In the USA this is used alongside BlightCase (farmers send environent variables like temperature, pH etc and are given a severity level based on where they live)
c) Simcast;data is input like time since last spray, spray frequency etc to give details about expected disease development levels
d) BlightPro: uses blightcase to decide to decide when to start spraying and SimCast to decide spray frequency
e) PLANT-plus: uses weather forecasting, disease models etc. studies show it is as good as a regular control programme for suppressing disease, but uses less spray
2) forecasting based on the amount of initial inoculum present

there is evidence that these systems work, but uptake has been limited: peoples livelihoods are at stake so farmers use fungicides curitively

35
Q

what is biologic control and what its advantages compared to chemical control

A

using microorganisms which are antagonistic towards pathogens

  • less ocstly
  • less environmental damage
  • less issues of resistance?
  • focus on soil bourne diseases because many microbes can establish themselves in the rhizosphere; this is good because chemical control molecules arent trasnported to the roots

-still novel and not used much but has potential

36
Q

what are the problems with biological control

A
  • possibility of resistance
  • some microbes produce compounds which are toxic to non-target organisms
  • not consistent; P. florescens was used to control take-all disease but only worke din 6/10 times in trials
37
Q

which factors promote success for biological control microorganisms

A
  • ability to become established and colonise the environment, for example have rhizosphere competence)
  • an ability to survive adverse environmental conditions for example by using resting structures such as spores
38
Q

what is the current status of biological control

A
  • 2005: 41 methods registered, half are ture fungi, half bacteria
  • still novel
  • many used for seed treatment: protect plant during its vulnerable stage until it can protect itself
39
Q

what are the 5 modes of action for biological control organisms

A

1) competition; outcompete pathogen near site of interest, for example competition for nutrients in the soil
2) antibiotic production against pathogen. ahrd to demonstrate antibiotic production in vivo however genetic studies help provide evidence and technology to detect small amounts of antibiotic in the field
3) parasitic action against pathogen
4) inducing host resistance
5) cross protection: use a mildly pathogenic strain of the pathgoen as inoculum against severe strain

40
Q

an example of biological control

A

disease: crown gall disease
pathogen: A. tumefaciens
control: Agrobacteria radiobacteria K1026
How:
-A. radiobacter K84 produces antibiotic Agrocin 84 which kills A. tumefaciens
-antibiotic action by inhibiting a tRNA
-mutation meaning pathogen couldnt take up the antibioitc would mean the bacteria would lose pathogenicity
-Plasmid from K84 was mutated so the plasmid cant be transferred to other microbes (known as K1026); this is essential because the plasmid contains genes for antibiotic resistance
-plant roots are wet with a bacterial suspension containing K1026
-very specific action; not many microbes take up the antibiotic

41
Q

discuss supressive soils

A
  • an example of biological control
  • soils where the pathogen inoculum is present but disease levels remain low
  • G. graminis damages root systems and causes take-all disease in wheat (less grain)
  • after 5 years of growing wheat, the severity of take-all increases but then stabilises to a low level; it is thought that antagonistic populations of microbes build up
  • aims to identify which species are in these poopulations so they can be added to soils
  • P. seudimonas is thought to be one; produced Phl antibiotic
  • experimental evidence supports their role; introduction led to lss take-all
  • perhaps the Phl genes can be added to other strains
  • Phl is non specific and can effect other plants so may not be commercialised (cucumber seeds show abnormal growth)
42
Q

how can biological control be improved

A
  • improve methods of application so organisms can better establish themselves
  • ontain better biocontrol organisms, for example by genetic screening
  • use an integrated approach of biocontrol organisms
43
Q

how do pathogens cause disease

A
  • divert nutrients
  • produce effectors (molecules which alter plant function such as defence mechanisms)
  • damage structural integrity; rot tissues and cell walls
  • cause abnormal development by latering hormone production/producing plant hormones
44
Q

how to pathogens infect plants

A

Root: when root goes near to the pathogen, chemical and electrical signals from root are used to locate host and germinate
-tends to be oomycetes (zoosproes so can swim to the root) or true fungi (have spores which germinate and form hyphae which move towords the root)

shoot: spore/sporangium land on lead, germinate andthen infect the plant via the stomata or directly through epidermis

45
Q

difference between true fungi and oomycetes in terms of spores

A

true fungi have spores

oomycetes have sporangium

46
Q

explain how spores gain entry to plants via leaves

A

1) initial attachment to leaf surface via hydrophobic interactions
2) imbibition occurs for 20 minutes; dried out spore absorbs water
3) formation of adhesion pad using carbohydrates and glycoproteins which secures the spore to the surface
4) release of enzymes like cutinase to loosed leaf surafce
5) seed germination (growth then pore opening causing material to flow onto leaf surface
6) hypha leaves spores and grows along the leaf before penetrating through the leaf

47
Q

after a hypha has left the spore attached to a leaf, describe how it penetrates the leaf

A

indirectly: grows through stomata which is found by detecting ridges on leaves (grow perpendicular to ridges), when a stomata is found an appressoria

directly: penetrate through cuticle
another structure called an appressorium forms which the spore empties itself into ebfore the appressorium produces a penetration peg which punches through the cuticle with. The pressure can be generated by the peg is due to its strengthened wall (melanin) and accumulation of glycerol to protect itself against osmotic stress
albino mutants (no melanin) cant accumulate glycerol and therefore collapse due to osmotic pressure

others use chemical methods of penetrating directly (enzymes) rather than mechanical force

48
Q

exmaples of species which penetrate leaves directly and indirectly

A

indirectly: U. viciae-favae
directly: M. oryzae

49
Q

how do biotrophs damage plants

A

formation of haustoria (a structure which grows into host cells without killing them and transports nutrients into itself via transporters)
transporters work by creating a proton gradient so that protons move into haustoria along with nutrients

50
Q

what are toxins

A
  • toxic dmagaing effect
  • small molecules (not usually proteins)
  • may help pathogen attack the host or contribute to symptoms
51
Q

what are the two types of toxins

A

host selective: only damage plants which is causes disease to
non-host selective: can damage plants other than those it causes disease to

52
Q

name a species which produces host selective toxins

describe the study done on it to prove the inmportance of toxins

A
  • Bipolaris
  • B. victoriae prodcues victorin toxin and causes Victoria blight of oats
  • B. zeicola produces HC-toxin and causes leaf spot of maize
  • progeny either produce no toxin, one toxic or both toxins
  • those proding victorin could attack oats, those who produced HC-toxic could attack maize etc
  • toxin is essential to pathogenicity
53
Q

describe HC toxin

what is the victorin mode of action

A
  • inhibits histone deacetylase (enzyme needed to turn on gene epxression in eukaryotes)
  • some maize are sensitive, some arent
  • resistence due to detoxification (Hm1 gene codes for Hc-toxin reductase)

victorin causes the plant to respond with an extreme defence mechanism which causes it to die

54
Q

what is the difference between pathogen and non pathogenic strain

A

pathgoen strains have genes for enzymes not found in non-pathogenic strains
genes are from horizontal gene transfer

55
Q

discuss a study which revealed how many genes are involved in pathogenicity

A

M. oryzae library of mutants was formed

of the 21,000 mutants, 600 had defective pathogenicity (200 genes identified)

56
Q

what is durable resistance

A

resistance which can be widely used for many years and remains effective

57
Q

what are the catagories of resistance (4 ways to group resistance)

A

preformed (resistance compounds present before infection) vs induced (plant responds with resistance upon contact to pathogen)

localised vs systematic

complete vs partial and everything in between

monogenic (single gene) vs polygenic (multiple genes)

58
Q

what are three mechanisms of preformed resistance

-add 3 examples

A
  • production of inhibitory substances
  • -white onions are more suceptible to onion smudge than other onions due to lower concentrations of phenolic compounds

-deactivation of pathogen enzymes and toxins

  • mechanical barriers to prevent access; thick cuticle, thick cell walls
    • older sycamore leaves are more resistant than new ones
  • -mandarin oranges are resistant to diseases that other citrus fruit arent due to very tight stomata which prevents water access
59
Q

what are the four mechanisms of induced resistance

A

1) localised cell death (hypersensitive response) to prevent pathgoen becoming established. occurs due to ROS such as hydrogen peroxide and capsases
2) synthesis of antipathogenic compounds such as phytoalexins. grape phytoalexin synthesis gene (stilbene) transfered to tobacco and confered resistance to grey mould
3) synthesis of antipathogenic proteins (pathogenisis related proteins) such as chitinases

4) strengthening of pre-existing structures like cell walls;
- -rapid deposition of callose (wound healing protein) at penetration site cells
- -gradual increase in lignification of cell walls over time

60
Q

describe monogenic vs polygenic resistance

A
  • monogenic
  • single gene
  • complete/no resistance
  • not durable
  • gene for gene interaction theory
  • polygenic
  • many genes
  • rarely complete resistance
  • durable
61
Q

disease terminology (avirulent etc)

A

resistant host: avirulent pathogen; incompatible

susceptible host; virulence host; compatible

62
Q

describe gene-for-gene theory

A

each resistance gene corrosponds to an avirulence gene

mutation of avirulence (dominant) gene causes virulence

avirulence gene binds to resistance gene causing a cascade of events leading to resistance

63
Q

explain how gene interactions occur

A

if the R-A interaction occurs (resistance gene and avirulence gene) it wins over a r-a interaction (susceptible and virulence gene)

64
Q

describe the first experiment demonstrating gene for gene interactions

describe another experiment showing gene-for-gene interactions

A

DNA from P. syringae pathovar glycinea strain psg6 (incompatible) was transfered to strain Psg1 (compatible) leading to the strain becoming incompatible against soybeans (Glycine max)
demonstration of gene for gene interactions
1984
arvA gene

Passalora fulva causes tomato leaf mould (Cf-9 tomatoes) from extracellular growth.
extracellular fluid of susceptible plants was extracted and applied to resistant plants; necrosis induced.
polypeptide known as avr9 later identified as the avirulent gene (disruption caused virulence)

65
Q

describe an experiment which eluded the function of a plant R gene

A

the plant R gene which confers resistance to P. syringae with Avr9 is called Pro

mutagenesis effecting Pro caused susceptibility to those with Avr9

66
Q

what are the 4 catagories of R genes

A
  • NBS-LRR
  • intracellular
  • nucleotide binding sites
  • leucine rich repeats which are involved in recognition

-LRR
-membrane spanning domains; extracellular binding
Cf-9

  • protein kinases
  • Pto (pro is a spelling error)

those with extracellular LRRs, membrane spanning domains and protein kinases

67
Q

discuss non-specific recognition

A

1) plant can recognise non specific pathogenic molecules (elicitors/PAMPS) such as cell wall fragments, flagellin (bacteria) and chitin (fungi) using PRRs (pattern recognition receptors)
2) a MAPK signalling cascade leading to phytoalexin production and HR response

(pathogenic associated molecular patterns)

many PPRs exist; absence of one doesnt result in compete susceptibilty

68
Q

discuss flagellin as an elicitior

A

non-specific recognition
bacteria were killed and boiled and applied to tomato plants leading to necrosis

the flg22 part of the protein is responsible (22AAs long)

the flagellin receptor gene has LRR`s, NBS and protein kinase domains

known as PAMP triggered immunity (PTI)

69
Q

difference between elicitors and effectors

A

elicitorsare those that cause non-specific responses in plants

effectors are toxins use to interfere with plant defence mechanisms

70
Q

how do pathogens overcome plant defence mechanisms

A

using effecotrs (toxins which interfere with plant defence mechanisms)

Type III secretory system in bacteria for example

71
Q

what is the zigzag model

A

describes how evolution between plants and pathogens

The plant detects pathogen PAMPS and performs PTI. the pathogen evolves effectors to interfear with PTI. eventually the effectors are recognised and responded to (now an avirulent gene) so
natural selection for mutated effectors which don’t trigger

72
Q

what is the guard hypothesis

name an example

A

the idea that perhaps there isint always a direct interaction between avirulence genes and resistance genes.

the R gene guards a protein which is the target of the effector and stimulates defencive responses

different effectors can act on the same target, which can be protected by multiple guards

1) P. syringae secretes an enzyme (AvrRpm1) which phosphorylates a plant protein (RIN4) and prevents the HR response from happening (non-specific response)
2) the plant has a guard mechanism; recognises phosphorylation using an enzyme (RPM1) and causes HR defence response
3) the pathogen secretes another protein (AvrB) which rephosphorylates the protein at another location causing HR suppression once more; plant defence stopped allowing it to be attacked

73
Q

what are RXLR proteins

A

oomycete pathogen elicitors
INF1 is an example; when secreted by P. infestans it is recognised and causes HR

sometimes pathogens have other effectors which supress cell death after INF1 recognition

74
Q

discuss victorin as a toxin

A

produced by B. victoriae

victorin can have toxic effects on oats and arabidopsis

binds to a plant enzyme (Trxh5) and prevents a defensive response
LOV1 gene has a guard role and causes HR

victorin is a diffusable substance so causes entire leaf death

B. victoriae feeds on dead tissue

75
Q

whats the difference between systemic acquired resistance (SAR) and induced systemic resistace (ISR)

A
  • systemic acquired resistance
  • when a single lesion casues widespread resistance which is effective against a range of pathogens
  • involves pathogenesis related proteins (PR proteins), which are those used in the local response
  • defence responses become primed; a quicker HR could occur if needed
  • signalling involving Salicylic acid
  • has potential in terms of immunising plants; activate plant defences using chemicals
  • induced systemic resistance
  • plant response involving jasmonic acid and ethylene signalling which is activated by treating plant roots with pathogens
76
Q

how can durable resistance be achieved

limitation of approaches

A

1)use polygenic resistance because it cant be overcome by a single mutation
limitation
-complicated for plant breeders
-marker assisted selection makes this approach easier (each gene is known as a QTL and has a quantifiable contribution to resistance); genes can be identified by markers such as SSLPs (single sequence repeat length polymorphism) or SNPs (single nucleotide polymorphisms)

for example if plant 1 has high quality geain but plant 2 has resistance genes then the cultivars are bred and offspring with the plant 1 genome as well as the resistacne gene was selectd using markers for the resistance gene

2) use monogenic reistance when it is appropriate
- when gene for gene interactions dont occur so the gene cant mutate to virulence
- when mutation of the avirulence gene reduces fitness so doesnt occur
- potantial for variation in avirulence gene is limited

77
Q

what is pre-emptive breeding

A

collect pathgoen and see which apthotypes are present (which hosts are susceptible) so resistant cultivars can be selected for the growing season

78
Q

where do resistance genes come from

A

wild relatives of the cultivar
cultivars cant be used for grain because they have undesirable genes linked to their resistance genes (fruit are hard etc); linkage drag

79
Q

what are 3 approaches for improving resistance

A

1) chemical induction of resistance
2) use marker assisted selection to transfer resistance genes to crops
3) use GM to introduce resistance; introdce PRR genes

80
Q

describe using GM to achieve resistance to late blight

A 
wild potato (S. bulbocastanum) gene for broad spectrum resistance (Rpi-blb1) was introduced into cultivated potato and tomato 
field testing showed success
project abandoned due to lengthy process of commercialsiation

later a gene from another wild relative was introduced to potato; commercialisation in 2017 and no virulent strains of P. infestans exist yet

plant biology 3 (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions