Basal Plant Immunity Flashcards

1
Q

What are the main aspects of plant innate immunity?

A

Recognition of pathogens via immune receptors and cellular polarisation to localise defence systems at infection sites.

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2
Q

What is the main challenge faced by global food security?

A

Plant pathogens

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3
Q

How do global trade routes affect global food security?

A

Distributes pathogens into regions of the world where plants are not adapted to that particular strain - worldwide effects as many countries are reliant on imported foods.

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4
Q

Give examples of organisms that can infect plants.

A

Bacteria, viruses, oomycetes, fungi, nematodes, insects and parasitic plants.

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5
Q

What are plants mainly infected by?

A

Filamentous plant pathogens - oomycetes and fungi.

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6
Q

What conditions are optimal for fungi and oomycete infection?

A

Humid conditions

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7
Q

Give the 3 ways in which filamentous plant pathogens can penetrate plant cells.

A
  • Through natural openings, e.g. stomata or wounded tissue.
  • Breaching the cuticle and penetrating between plant cells.
  • Breaching the cuticle and the cell wall to directly penetrate epidermal cells.
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8
Q

Give an example of a destructive crop disease.

A

Potato blight - caused by Phytophora infestans.

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9
Q

What are hyphae?

A

Penetration hyphae allow pathogens to penetrate between plant cells, and continue to grow within the apoplast.

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10
Q

How can hyphae penetrate individual plant cells?

A

Through the formation of haustoria.

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11
Q

What is the apoplast?

A

Extracellular space - hostile environment that contains hydrolases and is very acidic. Most invading bacteria will die in the apoplast.

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12
Q

What are haustoria?

A

Hyphael extensions that penetrate individual plant cells, and secrete virulence factors into the plant cell. Also absorb nutrients from the plant cell.

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13
Q

Describe focal immunity in plants.

A

Actin cytoskeleton rearrangement allows movement of the nucleus to the site of infection, as well as movement of vesicle machinery. This means that defences genes can be locally expressed and released. Vesicles deposit callose at the site of infection.

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14
Q

What are papillae?

A

Localised thickening of the cell wall at the site of pathogen contact, where there is accumulation of callose, phenolic compounds, arabinoxylan and cellulose.

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15
Q

What is the final component of papillae?

A

Cellulose.

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16
Q

What is callose?

A

Glucose polysaccharide, linked by B-1,3-glycosidic bonds - is the main component of papillae.

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17
Q

What happens if an ineffective papilla forms?

A

Lower levels of callose and arabinoxylan deposition and less cross-linking of polysaccharides. Penetration peg overcomes papilla and a haustoria forms, and the papilla shrinks. Pathogen secretes virulence factors that cause the plant cell to return to normality.

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18
Q

What is meant by ‘focal immunity is suppressed during susceptibility’?

A

All organelles and components of vesicle transport machinery return to the normal state, as a result of pathogen virulence factor action, and there is no secretion of defence molecules at the haustoria.

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19
Q

Can focal immunity be effective against adapted pathogens?

A

Yes to an extent - some cannot penetrate the papillae.

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20
Q

What is the extrahaustorial membrane?

A

A host-derived membrane, with different protein/lipid composition to the plasma membrane, that separates the haustoria from the remainder of the plant cell.

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21
Q

Give examples of hydrolases secreted by vesicles that are targeted towards haustoria.

A

Proteases, lipases, chitinases and nucleases.

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22
Q

What happens when P. infestans zoospores fail to germinate?

A

Plant cell has successfully prevented pathogen penetration and undergoes apoptosis - killing both the pathogen and the plant cell, but protecting the rest of the plant tissue.

23
Q

Is the callose barrier an effective protective mechanism against P. infestans?

A

Yes - approximately 30% of zoospores will be eliminated by this defence.

24
Q

Give an example of a bacterial crop disease.

A

Xanthomonas - causes brown spot disease in tomato plants.

25
Q

How do bacteria colonise plant tissue?

A

Through natural openings.

26
Q

Describe bacterial infection in plants.

A

Bacteria remain in the apoplast and use T3SS to secrete effectors into the plant cell. VFs must be unfolded to pass through T3SS - these are folded by the plant cell machinery and act upon different organelles in the plant cell. Some effectors target vesicle transport routes to disrupt focal immunity.

27
Q

How can a plant be resistant to bacteria?

A

By having intracellular NLRs against the bacterial effectors, which activate programmed cell death (HR).

28
Q

Why are white lesions seen on the leaf surface of plants showing pathogen resistance?

A

Indicates site of infection, as there has been programmed cell death and there is no longer any chlorophyll present.

29
Q

How are most invading pathogens eliminated in plants?

A

By pre-formed barriers and focal immunity - immediate innate responses.

30
Q

Give the two types of induced innate immunity in plants.

A

Local defence and systemic defence.

31
Q

Describe the local defence of induced innate immunity in plants.

A

Relies on early detection of the pathogen and results in the production of defence molecules. Restricts pathogen growth and spread - infected cells undergo apoptosis and the remainder of the plant tissue is saved.

32
Q

Describe the systemic defence of induced innate immunity in plants.

A

Protects non-infected tissues from secondary infection, giving the plant increased resistance. Mechanisms are not yet understood.

33
Q

How are pathogens detected in plant cells?

A

PRR recognition of PAMPs.

34
Q

What is the advantage of PAMP recognition?

A

Requires genome to encode fewer receptors, and enables widespread recognition of pathogens.

35
Q

Give the general features of PAMPs.

A
  • Conserved; widely or narrowly.
  • Required for the general lifestyle of the pathogen, not necessarily involved in virulence.
  • Secreted by pathogen or released upon pathogen death.
36
Q

How can DAMPs trigger an immune response?

A

DAMPs released by plant cells during pathogen-induced cell wall/cuticle damage can be recognised by PRRs.

37
Q

Give the 3 types of surface immune receptors in plant cells.

A
  • Receptor-like kinases (RLKs)
  • Receptor-like proteins (RLPs)
  • LYSm domain receptors.
38
Q

Describe receptor-like kinases.

A

Have LRRs for PAMP recognition, and kinase domains for triggering downstream signalling. Usually ser/thr kinase.

39
Q

Describe receptor-like proteins.

A

Have LRRs for PAMP recognition. Have a short cytoplasmic domain, with no kinase domain.

40
Q

Describe LYSm domain receptors.

A

Involved in symbiosis and immunity. LYSm domain binds chitin and peptidoglycans. Has an intracellular kinase domain – usually ser/thr kinase.

41
Q

How does EF-Tu meet the requirements of being a PAMP?

A
  • required for protein translation in bacteria
  • highly abundant
  • released when bacteria die in the apoplast
  • conserved residues at the N-term
42
Q

Why is it thought that the EFR evolved recently to recognise EF-Tu?

A

Only present in Brassicacae family of plants.

43
Q

How can tomato plants be given resistance to bacterial infections? What does this indicate?

A

By provision of the EFR - allowing recognition of bacterial EF-Tu. This suggests that downstream signalling of PRR-triggered immunity is conserved in plants.

44
Q

How does flagellin meet the requirements of being a PAMP?

A
  • required for motility
  • secreted
  • highly abundant
  • highly conserved
45
Q

What is recognised by FLS2?

A

The flagellin Flg22 epitope.

46
Q

What happens upon PRR activation?

A
  • Massive production of ROS (within 15 minutes)

- Reprogramming of gene expression

47
Q

Describe the changes in gene expression that occur following PRR activation.

A
  • activation of defence genes
  • repression of genes that inhibit defences
  • expression of defence hormones involved in systemic defence
  • production of callose
48
Q

Describe the role of guardee proteins in PRR-triggered immunity.

A

Bind effectors, and this is then recognised by RLPs, triggering the hypersensitive response.

49
Q

Compare PRR-triggered immunity and the hypersensitive response.

A

PRR-triggered immunity is milder than HR and does not normally result in plant cell death.

50
Q

Give the roles of ROS production during PRR-triggered immunity.

A
  • antimicrobial; inducing oxidative stress in pathogen.
  • aids cell wall cross-linking at papillae.
  • stimulates stomata closure to prevent pathogen entry.
51
Q

Describe the signalling downstream of FLS2.

A
  1. FLS2 activated by flagellin.
  2. FLS2 forms a complex with BAK1 - transautophosphorylation.
  3. BAK1 recruits BIK1 kinase and activates STP13.
  4. BIK1 kinase activates RHOBD.
52
Q

What is RHOBD?

A

NADPH oxidase - produces superoxide from molecular oxygen, which can then spontaneously dismutate to give hydrogen peroxide. ROS released into the apoplast.

53
Q

What is STP13?

A

A surface localised sugar transporter. Expression is upregulated during infection.

54
Q

How does STP13 activity contribute to the killing of bacteria in the apoplast?

A

STP13 brings sugar into the plant cell from the apoplast - depriving bacteria of their energy source.