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Sem 1: Plant Biology > Week 11 > Flashcards

Week 11 Flashcards

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1
Q

What are the big three plant sources of food?

A

Wheat, maize and rice

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2
Q

What are some of the many uses of maize (corn)?

A

1/3 of all corn grown in the US is used to feed farm animals
Corn starch is used as a bonding agent is aspirin tablets
Corn starch helps lubricate plastic molds so individual parts can be easily removed

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3
Q

Where does cereal crops in the EU go?

A

62% used in animal feeds
23% feeds people
12% used in industry and biofuels

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4
Q

What are the percentages of crop food waste?

A

35% - Pre-harvest
16% - Post-harvest
23% - Animals
26% - Remaining

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5
Q

What are examples of pre-harvest challenges?

A

“Imperfect” or surplus
Abiotic stress
Biotic stress

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6
Q

What are examples of post-harvest challenges?

A

Transport
Storage
Processing and packaging
Food thrown
Expired before sale

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7
Q

What caused the great famine in 1840s Ireland?

A

An outbreak in potato late blight, caused by Phytophtora infestans (Oomycete)

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8
Q

What is the historical context for the discovery of the potato late blight?

A

Potatoes were bought to Europe to South America starting in the 16th century, but the pathogen Phytophthora infestans was not observed in Europe until the 19th century

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9
Q

How much loss of Rice yield is caused by RIce blast disease?

A

Rice blast caused upto 30% yield loss of rice every year

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10
Q

Where did wheat blast start?

A

1985 in South America

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11
Q

Where did wheat blast travel to after starting in South America?

A

Bangladesh 2016
Zambia 2018

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12
Q

How does Fusarium graminearum (not wheat blast) threaten plants?

A

It is a nectroph pathogen which uses mycotoxins

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13
Q

What is important to know about the mycotoxins used by Fusarium graminearum?

A

It can spread to people though consumption or comsumption of meat which allows the toxin to build up

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14
Q

What are the pre-harvest strategies for reducing mycotoxins?

A

Plant protection during vegetation: agronomic, chemical and biological methods

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15
Q

What are the post-harvest strategies for reducing mycotoxins?

A

Physical, chemical and biological methods

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16
Q

What are the 4 classifications of plant pathogens?

A

Necrotroph, biotroph, symbiont and hemi-biotroph

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17
Q

What are necrotroph?

A

Pathogens that kill plant cells, causing plant tissues to rot
This is seen in Botrytis cinerea (fungus)

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18
Q

What is a biotroph?

A

Pathogens that absorb nutrients from the plant but dont kill any cells.
This is seen in Ustilago maydis and Cladosporium fulvum

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19
Q

What is a symbiont?

A

A pathogen that has formed a symbiotic relationship
This is seen in Rhizophagus irregularis and Laccaria bicolor

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20
Q

What is a hemi-biotroph?

A

A pathogen that initially just steals from plant and keeps cells alive in the biotrophic phase but will kill the cell in the future in the necrotropic phase
This is seen in Magnaporthe oryzae

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21
Q

What is the lifecycle of the fungal pathogen Magnaporthe oryzae?

A

A conidium (spore tip) attatches itself to a plant
It then sprouts a germ tube
This then forms a melanin-lines appressorium cell wall
The appressorium then penetrates the cell wall of the plant
This develops into a primary invasive hyphae, which steals resources from the cell
Then tissue colinisation will occur as the fungus infects other cells
Then a conidophore sprouts from the plant releasing more conidium

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22
Q

What is appressoria?

A

A specialised cell generating enourmous turgor pressure aroun 8 Mpa

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23
Q

How do oomycetes invade host cells?

A

They invade host cells at an oblique angle without forming a melanised appressoria

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24
Q

How does the hyphae reduce chances of the immune system finding it?

A

It is surrounded by a plant plasma membrane

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25
Q

What is a haustoria?

A

A protrusion of invasive hyphae as an interface between the pathogen and plant

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26
Q

What are effectors in plant biology?

A

Effectors are proteins expressed by plant pathogens to aid infection of specific plant species

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27
Q

Where does effectors impact?

A

Effectors are secreted proteins which can be translocated into plant cell cytoplasmic, or into apoplatic space

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27
Q

Where do effectors impact?

A

Effectors are secreted proteins which can be translocated into plant cell cytoplasmic, or into apoplatic space

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28
Q

What is the function of effectors on the plant cell cytoplasm or apoplatic space?

A

They can manipulate plant physiology and hijack the plant immunity response

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29
Q

What are the two types of effectors?

A

Cytoplasmic effectors and Apoplastic effectors

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30
Q

What is one of the typical features of a oomycete effector?

A

RXLR motif

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31
Q

What secretes apopletic effectors of filamentous pathogens?

A

This is done via the conventional ER-to-Golgi

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32
Q

When does necrotrophic growth occur?

A

When the plant cell loses viability

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33
Q

Why is wheat important?

A

2nd biggest supplier of calories for human consumption
Grown in biggest range of Agro-ecological environments 67 N (Norway) to 45 S (Argentina)

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34
Q

What are the two types of wheat?

A

Triticum durum (pasta wheat)- Tetraploid AABB
Triticum aestivum (bread wheat)- Hexaploid AABBDD

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35
Q

How did wheat evolve?

A

Wild Einkorn and a goat grass with a doubling of chromosomes forming Emmer Wheat. An another grass (Aegoliops squarrosa) was added giving genes that make glutenins, bread that rise

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36
Q

When did wheat reach the British isles?

A

Iron age (pre-Roman)

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37
Q

What are landraces?

A

The breeding of crop varieties adapted to local conditions, through years of natural and human selection

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38
Q

Who invented the seed drill?

A

Jethro Tull

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39
Q

Who pioneered selective crossing?

A

Bateson and Biffin

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40
Q

What are the advantages of selective crossing?

A

Improved disease resistance
Better yield
Better bread-making quality
Bought in genetics (Ghirka- yellow rust resistance from Russia and White fife- bread making from Canada)

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41
Q

What is the method of selective plant breeding?

A

Multiple crosses from parents with intesting characters
F2 generation screened by eye

42
Q

What generation of selection does commercial use start?

A

F12

43
Q

Who discovered the Norin 10 gene?

A

Norman Borlaug

44
Q

What is the advantage of Norin 10 gene?

A

Semi dwarf gene, stiffer straw, plant height halved from older varieties which lodged (fell over)

45
Q

How did the Norin 10 gene impact harvest index?

A

Modern varieties have HI over 50%

46
Q

What are the problems of major genes for disease resistance?

A

Often 1 gene so quickier for diseases to evolve around the impact of the gene

47
Q

What is the ideal time for winter wheat sowing?

A

Sept to November

48
Q

What is the ideal ear to m2 number?

A

800 ears per m2

49
Q

What are the yield components of wheat?

A

Tillers/ears
Spikelets per ear
Grain sites per spikelet
Grain fill

50
Q

What is the theoretical maximum yield in the UK?

A

~25 tonnes/ha
Highest achieved 16.5 t/ha
Average 8 t/ha

51
Q

How can we increase wheat yields?

A

Appropriate soil cultivation
Effective weed control
Prevent aphids transmitting virus into crop (in BYDV crop)
No root damage by fungi or insects
No winter damage (hard frost or rotting under snow cover)

52
Q

How can we look after wheat?

A

Apply sufficient Nitrogen and sulphur during March/April
Apply straw stiffeners
Normally 3 doses of fungicide (product mix to avoid fungal resistance)
Hope it doesnt rain too much

53
Q

What unknows are their in crop management?

A

Trace element effects
Elicitor response for disease management

54
Q

What are the targets for the future to increase crop yields?

A

Nitrogen uptake - 50% applied is recovered in grain
Better understanding of root rhizosphere population interactions (wheat not a strong interacter with Mycrohizia)
Improve disease resitance - gene editing
Improve breadmaking quality - gene editing

55
Q

What is way out there in the future for improving wheat yields?

A

Nitrogen fixing wheat
C4 photosynthetic wheat

56
Q

How can wheat be redesigned for vertical farming?

A

Full dwarf
Less need to worry about disease (sealed environment)
Optimise plant/light spectrum interaction
4% water usage of field crop - more likely in arid areas with good solar power source

57
Q

What is the difference between wild plants and agricultural plants?

A

Most wild plants are resistance to most pathogens compared to agcriculture which is more prone due to growing crops as monocultures

58
Q

What are the 5 main types of plant pathogens?

A

Fungi
Nematodes
Oomycetes
Viruses
Bacteria

59
Q

How much of global crop yields are lost by pests and diseases?

A

20% to 40%

60
Q

What are the 4 major diseases causing crop loss?

A

Blast disease (fungus)
Smut disease (fungus)
Fusarium head blight disease (fungus)
Rust disease (fungi)

61
Q

What do the 4 major diseases causing crop loss infect?

A

They all infect grasses

62
Q

How long have humans been dealing with plant diseases?

A

Since start of agriculture

63
Q

How did humans in early stages of agriculture attribute with plant diseases?

A

They were attributed to the supernatural- Demeter and Robigus roman god of wheat
People sacrificed dogs to Robigus to prevent red dust (rust disease)

64
Q

How did medieval people believe was the cause of Ergot poisoning from eating infected Rye by fungus?

A

This led to people having siezures but people believed it was caused by the devil possessing people

65
Q

Who and when was the first microscope invented?

A

Anton von Leeuwenkoek in 1683

66
Q

What was Miles Joseph Berkely work?

A

Founding father of british fungal research
He proposed that plants were sick because of the mold rather than the mold being their as the plant is sick

67
Q

What are the 3 components of plant disease triangle?

A

Plant- host plant must be susceptible to the pathogen
Pathogen- pathogen must be able to overcome plant defences
Environment- Must tip the balance in favour of the pathogen

68
Q

Using the 3 components of plant disease triangle how can you manage and prevent plant disease?

A

Host- Make the plant resistant to the pathogen through breeding
Pathogen- Minimise or eliminate the prescence of the pathogen
Environment- Manipulate the environment to favour the plant and not pathogen

69
Q

Compared to animals what type of immune system to plants have?

A

They only have an innate immune system

70
Q

What is the core statement for plant immune system?

A

Plants resist pathogens through pathogen recognition and followed by defense responses to fight them

71
Q

What are the two branches of plant immune system?

A

First branch: Defenses outside the plant cell
Second branch: Defenses inside the plant cell

72
Q

What is the first stage of plant immunity?

A

Pattern-Triggered immunity (PTI) recognises the MAMPs/DAMPs that are secreted by the pathogens. The MAMPs/DAMPs are recognised by cell-surface receptors

73
Q

What are cell-surface reptors also called?

A

Pattern recognition receptors (PRR)

74
Q

What part of the PRR is involved in MAMPs/DAMPs recognition?

A

The extracellular leucine-rich repeat domain

75
Q

What are the 3 parts of the PRR?

A

The extracellular leucine-rich repeat domain. transmembrane domain and intra-cellular domain

76
Q

What is the function of the intra-cellular domain?

A

They carry on the signal for recognising the MAMPs/DAMPs

77
Q

What does PAMPs stand for?

A

Pathogen Associated Molecular Patterns

78
Q

What is the name of the PAMPs and the Leucine-rich repeat receptor kinase PRR that recognises it?

A

Flagellin = FLS2
EF-TU = EFR
Ax21 = XA21

79
Q

What is the name of the PAMPs and the LysM receptor proteins PRR that recognises it?

A

Chitin = CERK1

80
Q

How do plants respond to detection of PAMPs?

A

With a large scale trancriptional response

81
Q

What are the responses involved in large scale plant transcription from prescence of PAMPs?

A

Increase synthesis of stress hormpnes
Up-regulation of pathogenesis-related (PR) gene
Synthesis of antimicrobial compounds including phytoalexins
Production of reactive oxtgen species (ROS)
Production of polysaccaride callose (creates a membrane between cell membrane and cell wall)

82
Q

How did they increase pathogen tolerance for tomato plants?

A

The PRR EFR gene was introduced into the tomato, allowing for the plant to become resistant to a new pathogen due to new PAMP being recognised

83
Q

What is the second branch of plant immunity?

A

Effector-triggered immunity

84
Q

What is the benefit of microbial effectors?

A

They supress the plant immune system’s reponse and/or contribute to pathogen’s viability

85
Q

How does microbial effectors impact pathogen effectors?

A

Mitigate the first branch of the immune system

86
Q

How do nematodes introduce effectors?

A

They are introduced through the feeding stylet

87
Q

How are fungal and oomycete effectors introduced?

A

They are secreted from haustoria or tips of hyphae

88
Q

How are bacterial effectors introduced?

A

They are introduced through Type-III secretion systems (T3SS) or other secretion systems

89
Q

How are microbial effectors detected?

A

They are detected by the NLR proteins

90
Q

What are the three domains of plant NLRs?

A

TIR, CC and RPW8- Signal transduction (downstream communication of pathogen detection)
NB-ARC- On/Off switch
LRR- Pathogen recognition

91
Q

What happens in direct binding of pathogen effector?

A

When in off state the 3 domains are close together
On state effector binds to the LRR, so it opens up and become activated, triggering an immune response

92
Q

What happens in indirect binding of pathogen effector?

A

When in off state the 3 domains are close together
Effector binds somewhere else which is being monitored by the LRR, which then causes the NLR to open up and activate

93
Q

What happens when NLRs are active?

A

They form a funnel like structure called “resistosomes”. It its a protein complex

94
Q

What is the function of resistosomes?

A

It goes to the plasma membrane creating ion influxes enhances plant immune response

95
Q

How can NLR transferring benefit different species?

A

They transferred the wild potato confer NLR into farm potatoes giving domestic plants Potatoe late blight (Phytophthora infestans) resistance

96
Q

What is the zig-zag model of plant-pathogen interaction?

A

Pattern triggered immunity- pathogen recognised
Effector triggered suceptibility- effectors supress immune defence
Efector triggered immunity- effector is “recognised”

97
Q

What is the red-queen hypothesis?

A

Species must constantly adapt and co-evolve to remain competitive

98
Q

What are the key feature of NLRs?

A

They are highly diverse immune system components

99
Q

Why are animal NLRs receptors typically lower than in plants?

A

They bind to well conserved section of microbial effectors, more like PRRs, so they dont need to change as much

100
Q

How do NLRs vary across plants?

A

They are highly variable in both number and their sequence (more likely to detect effectors)

101
Q

What happens when you mix too many NLRs or PRR and NLRs?

A

This results in hybrid incompatibility (autoimmunity), due to highly upregulated genes to do with immune response, even when no pathogen

102
Q

What are the 2 main challenges to plant immunity?

A

Increasing food demand due to population rise and meat consumption
Climate change

103
Q

What are the 2 main opportunities to plant immunity?

A

Genomic and biotechnology tools to accelerate research and breeding
Improvements in education and for the public

Sem 1: Plant Biology (10 decks)

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