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L3 Plant Sciences > Week 15 L1: Plant-Microbes pt1 - PLANT > Flashcards

Week 15 L1: Plant-Microbes pt1 - PLANT Flashcards

1
Q

What are kinds of organisms which cause disease?

A 
nematodes 
viruses 
fungi 
bacteria 
Insects
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2
Q

What are nematodes?

A
  • are large, multicellular animals

- a worm of the large phylum Nematoda, such as a roundworm or threadworm.

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3
Q

What is a virus?

A

A virus is a submicroscopic infectious agent that replicates only inside the living cells of an organism.

are non-cellular, and merely packaged nucleic acids

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4
Q

What is the difference between fungi and bacteria?

A

bacteria is a prokaryote and fungi are eukaryotes

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5
Q

How does an insect spread disease?

A

Inject them into the plant tissue which they eat

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6
Q

What are viruses and their relatives?

A

viroids and phytoplasmas

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7
Q

What is a viroid? What do they not have which viruses do?

A

Viroids are very similar to viruses except that they do not have a protein coat, they are simply self-replicating and transmissible nucleic acid pathogens. Viroids are usually spread through aphids or mechanical transmission.

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8
Q

What is an aphid?

A

small sap-sucking insect

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9
Q

What is the phytoplasmas?

A

obligate intracellular parasites of plant phloem tissue and of the insect vectors that are involved in their plant-to-plant transmission.

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10
Q

What are the 3 factors a pathogen needs to overcome to cause disease?

A

environment, host and pathogen

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11
Q

Explain the 3 factors of the host triangle, which when overcome lead to disease?

A

Pathogen - the pathogen must be able to overcome the plants immune defence
Host - the host has to be susceptible to the pathogen
Environment - Must lean in favour of pathogen

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12
Q

When is the environment in favour of a pathogen?

A

e. g. drought, the plant will be stressed and more susceptible to the invading pathogen.
e. g. Humans play a role - farming environments.

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13
Q

What makes a successful pathogen?

A
  1. pathogenesis genes and effectors

2. numbers

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14
Q

Why do genes and numbers make for a successful pathogen?

A

genes - allow the pathogen to enter into the plant,
evade the plant’s defences, and survive
and reproduce

numbers - Increase chance of success. May need many spores to cause a successful invasion

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15
Q

What makes a vulnerable host?

A
  • Poor health – wounded or weakened plants can be more vulnerable
  • A lack of disease resistance gene
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16
Q

Why is a wounded more vulnerable to pathogen invasion?

A

immune response requires a lot of energy and most of its energy is in cellular repair.

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17
Q

What are effectors?

A

supress plants immune defences, release nutrients for their own survival and reproduction

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18
Q

What is a spore in a bacteria

A

outer shell, identified as a foreign pathogen in plants. It helps protect the bacteria in harsh conditions.

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19
Q

What is pathogenicity?

A

act of causing disease

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20
Q

What are the stages of a successful invading pathogen (pathogenicity)?

A
  • Find the host and attach to it
  • Gain entry through the plant’s impermeable defences
  • Avoid the plant’s defence responses
  • Grow and reproduce
  • Spread to other plants
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21
Q

What are ways a pathogen can enter a host?

A

The pathogen has structures to bypass the cell wall/cell membrane surface
The pathogen uses the plants natural openings e.g. stomata

22
Q

Does the plant have immune responses for the invading pathogen?

A

yes,
Plants resist pathogens through active processes that include recognition of the pathogen and defence responses to fight it.

23
Q

What is the zigzag model?

A

a simple coevolutionary model of plant–pathogen interactions, called the ‘zigzag’ model, which encompasses two branches of the plant immune system

24
Q

What is the first stage of the zigzag model?

A

Pathogen is recognised by pattern triggered immunity - trigger immune response

25
Q

What is the second stage of the zigzag model?

A

Pathogen effectors suppress

defence response: Effector Triggered Susceptibility

26
Q

What is the third stage of the zigzag model?

A

Effector is “recognized”: Effector Triggered Immunity

27
Q

What are the 2 stages of plant defence response?

A
  1. pattern triggered immunity

2. effector triggered immunity

28
Q

What does the zigzag model not take into account?

A

environment

29
Q

Are the 2 pathways in the zigzag model distinct?

A

NO, the downstream pathways of the 2 defence receptors overlap.

30
Q

What is an overview of plant-microbe interactions - ZIGZAG model?

A

PAMPs and MAMPs are recognised by PRR receptors on the cells surface, this initiates a PTI in the cell.

This PTI is repressed by effector cells from the invading bacteria, nematode etc. supress immune response

Resistant plants inhibit the effectors by inhibiting them with specific proteins called NLRs, this initiates a ETI.

31
Q

What are the proteins which inhibit effectors?

A

NLRs

32
Q

What part of flagellum binds to PRR?

A

flagellin globular protein, specifically the flg22 domain (motif)

33
Q

What receptor does flagellin bind to?

A

FLS2 PRR

34
Q

Is FLS2 an LRR?

A

yes - LRR receptor-like kinase

35
Q

What is flagellum?

A

filamentous protein structures found in bacteria, archaea, and eukaryotes, though they are most commonly found in bacteria
tail region of bacteria, used to propel through liquid

36
Q

What are the features of a PAMP region?

A
  1. Conserved across microbial genera e.g. flagellin
  2. Not required for infection, but important biological roles
  3. Not strictly found in pathogens (also other microbes)
  4. Often surface exposed
  5. Not present in the host
37
Q

What is another example of a bacterial PAMP that binds PRR?

A

EF-Tu

elongation factor

38
Q

What part of PAMP EF-Tu binds PRR?

A

Elf 18

39
Q

What receptor does Elf18 bind to?

A

PRR - ERF

40
Q

When PAMP binds a PRR, how does it initiate an immune response?

A
  1. KINASE CASCADE LEADING TO TRANSCRIPTION RESPONSE
  2. Calcium influx
  3. ROS production
41
Q

What can initiate a direct immune response and bi-pass transcription?

A

ROS production

42
Q

What are the plants chemical defences?

A

antimicrobial compounds; phytoalexins and phytoanticipins

43
Q

What is the difference between phytoalexins and phytoanticipins?

A

phytoalexins are induced metabolites

phytoanticipins are present in plants ta all times (pre-formed)

44
Q

What is the role of chemical defences?

A

toxic to pathogen

45
Q

What kind of metabolites are phytoalexins and phytoanticipins?

A

secondary - they are not involved in growth, photosynthesis, reproduction, or other “primary” functions.

46
Q

What is the effect of phytoalexin?

A

can contribute to their defence, raise the
nutritional quality of some foods, and
provide a source of human medicines.

47
Q

What is a secondary metabolite which is good for the aphid defence in Arabidopsis?

A

glucosinolate

48
Q

When is callose produced?

A

Change in gene expression and it is released form the golgi-mediated callose secretion

49
Q

What 3 compound are useful in arresting pathogen attack?

A

callose, phytoalexins and ROS

50
Q

What are the functions of ROS?

A

important in signalling and also toxic to pathogen

51
Q

What is the role of callose in arresting pathogen attack?

A

Its a polysaccharide and acts as a barrier to pathogen by imbedding in the cell wall.

L3 Plant Sciences (17 decks)

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