Plant Defence & Nitrogen Fixation Flashcards

1
Q

What are R proteins?

A

Products of R genes, part of plant immunity. (R for resistance)

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2
Q

What are biotrophic pathogens?

A

Parasitise living cells, hide and stay secret from plant. Feed on living plant tissue

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3
Q

What are necrotrophic pathogens

A

Digest cells with proteases. Feed on dead cell matter

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4
Q

What is the general rule for plant immunity?

A

Resistance to pathogen is the norm. Susceptibility to the disease is the exception.

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5
Q

How do R genes interact with pathogens?

A

Microbial pathogens have effector proteins which are the virulence factors which help to colonise the host. Products of R genes scan cells for these effectors, recognition of an effector triggers defence. This pathogen is now avirulent.

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6
Q

What is an avirulence (AVR) protein?

A

An effector protein which can be recognised by an R protein in the plant. Rendering the pathogen avirulent.

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7
Q

What is race specific resistance?

A

R Gene resistance is very specific to the pathogen race (race specific effector) and the plant cultivar (does it have a specific R gene to counter it)
Can cross R genes from wild species into commercial cultivars

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8
Q

What is the hypersensitive response?

A

In HR recognition triggers cell suicide resulting in execution of challenged cells. Removing nutrients from invading pathogens.
This only works against biotrophs as they need living cells.
Also includes ROI production (no clue no context on slides :((() and callose deposition to limit pathogen entrance before cell death

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9
Q

What are the purpose of effector proteins?

A

They aim to inactivate other defences such as the unspecific Pattern Triggered Immunity (aims to recognise general traits eg flagella amino acids)

Some also help with plant entry as P. Syringae effectors induce opening of stomata

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10
Q

Requirements of infection?

A

Pathogen must overcome defences
Plant must be susceptible
Environment must be tipped in favour of pathogen

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11
Q

What is a Hemibiotroph?

A

Can switch between necro- and biotrophic

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12
Q

Methods of pathogens entering plant?

A

Enter through stomata
Brute force with high pressure to puncture wall
(No mentioned in notes but also cellulases?, Need to break down cuticle first though)

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13
Q

How does unspecific recognition work?

A

Plant has cytoplasmic pathogen recognition receptors to recognise general proteins from pathogens (flagella proteins eg). They induce signalling causing expression of anti pathogen defences

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14
Q

What is some general R protein structure?

A

Nucleotide binding site (as they induce expression of other proteins)
LRR (Leucine rich repeat)

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15
Q

What is an effect of R protein activation?

A

Production of Salicylate (stress hormone)

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16
Q

Two types of system immunity in plants?

A

LAR: Local acquired resistance (just leaf is resistant)
SAR: Systematic acquired resistance (entire plant is resistant)

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17
Q

Difference between virulent and avirulent?

A

A pathogen is virulent if the plant doesn’t have recognition for it - and so is susceptible
It is rendered avirulent once the plant recognises it and it induces defences
Preinoculation of a plant with an AVR protein that it recognises can protect from subsequent infection

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18
Q

What is the biochemical basis of SAR

A

Involves group of SAR-Pathogenisis related proteins (PR-Proteins)
PR proteins accumulate in local and systemic leaves during SAR development
PR-2 encodes Glucanase
PR-3 encodes Chitinase
Others encode proteins of unknown function
Induction of SAR involves motile signal as uninflected tissue has enhanced resistance to subsequent pathogens

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19
Q

What is the order of a resistance response?

A

Resistance response triggers release of signal
Signal establishes LAR in local leaf
Signal exits local leaf and establishes SAR in all leaves

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20
Q

What does salicylate signal induce?

A

PR protein synthesis
SAR
It is a local signal for LAR , it is not the systemic mobile signal for SAR

21
Q

What does spray in with SA do?

A

Activated SAR genes
PR-proteins accumulate
SAR develops

22
Q

What are the 2 methods for inducing SAR?

A

Biological: inoculate with AVR protein
Chemical: spray with SA

23
Q

Downside of treating crops with SA?

A

Decreases yield if done constantly as immune response diverts energy away from growth :(

24
Q

What sort of plants associate with rhizobia

A

Legumes

25
Q

What is rhizobia?

A

Common soil bacteria, gram negative, induces root nodules inlegumes
Reduce N2 to ammonia which legume can use (triple bonded N2 too difficult for plant, Sad!)

26
Q

How do plants attract rhizobia?

A

Flavonoids (phenolic compound derived from phenolpropanoid pathway) are released from roots, chemoattractants for rhizobia, attract them into rhizoshere

27
Q

What are the 3 rhizobia genera

A

Rhizobium (grow fast)
Bradyrhizobium (slow)
Azorhizobium (free living)
NOT close related!!!!

28
Q

What are the functions of flavonoids?

A

Chemotaxis (attracting the bacteria)
Nod gene activation
Increased growth rate

29
Q

Haemoglobin in nodule?

A

Nitrogenase enzyme v sensitive to oxygen
Oxygen held away in haemoglobin to prevent inactivation

30
Q

What is nod D

A

Regulatory nod gene global activator of nod genes
Transcriptional activator
Helix-turn-Helix binding motif
Binds to conserved cis element NOD box present in promoters of all nod genes

31
Q

Nod D mechanism?

A
  1. Binds to flavonoid (early theory)
  2. Confirmational change to DNA bind form
  3. Binds to NOD boxes, nod gene expression activated

(My notes say GroEl and (p)pGpp are needed for NodD function, no clue if bullshit or not)

32
Q

What are the 2 host specific flavonoids for R. Meliloti

A

Luteolin and Alfalfa

33
Q

What are the common nod genes

A

Nod A, B and C
Easy peasy
All others are specific to certain cases

34
Q

What is a Nod factor?

A

Lipo Oligosaccharide produced by rhizobia which induce nodule formation in target

35
Q

What is the process from flavonoid in plant to nodule?

A

Plant root secretes flavonoid
Attracts rhizobia, other effects
Binds to NodD in rhizobia
NodD activated transcription of other Nod genes
Nod A,B,C synthesise core nod factor structure
Other Nod genes enable synthesis of specific nod factors
Nod factors secretes by rhizobia
Nodule formation induced in specific target legume

36
Q

How do roots and bacteria test compatibility

A

Flavonoid signalling and nod factor signalling are specific and so work between compatible species

37
Q

When does the symbiosis occur

A

Starvation events :,(
Individuals would rather be independent

38
Q

What is the nature of the symbiotic relationship?

A

Rhizobia induce symbiosis specific differentiation
Establishes a niche for the rhizobia
Rhizobia provided with photosynthate
Provide fixed nitrogen under n limiting conditions

39
Q

What is the first effect of nod factors on the plant?

A

Root hair curling
Induced root tip growth, resulting in curling and deformation
Rhizobia is trapped in the curl
May produce hydrolytic enzymes to degrade cell wall, facilitating entry

40
Q

Why do sym1 and sym5 mutants not form nodules in response to factor?

A

Encodes receptor like kinases
Both required for nod-factor recognition (work synergistically)
Designated NFR1 and NFR5 (Nod Factor Receptor)

41
Q

How does nod factor signalling work in L. Japonicus?

A

Extracellular NFR1 and NFR5 domain (are together in membrane) interacts w nod factor
Causes membrane depolarisation with ion flux
SYMRK then causes signalling into nucleus via calcium signalling into nucleus through nuclear membrane Ca transporters, regulates gene expression)
Root hair curling occurs
Infection thread formation
Nodule organogenesis

42
Q

Infection thread formation?

A

Plant P.M. invaginates
Rhizobia enters invagination
Cell wall material deposited around invagination to form infection thread
Infection moved through root hair and transverses root to reach root cortex
Thransferred to root cortex

43
Q

What are the two different nodule types?

A

Determinate nodules: infect outer cortex (L. Japonicus)
Indeterminate nodules: infect inner cortex (M. Truncatula)

44
Q

What does infection do to cortical cells (cortex)

A

Usually don’t divide, just transport water and such
Undergo differentiation before penetrated by infection thread
Nucleus moves to cell centre
Cytoplasm and endonembranes move to cell periphery
Cell forms a Phragmoblast
Thread releases some rhizobia into cell via endocytosis
Rhizobia become surrounded by a plant derived prebacterioid membrane
Bacteria are now differentiated into bacterioids

45
Q

How much ATP for nitrogenase to fix N2 to 2NH3?

A

16 MgATP (whatever that is lol)
(Reduction need 8H+ and 8e-)
Products are 2NH3, H2, 16MgADP, 16Pi

46
Q

What is a reason for rhizobacteria to maintain symbiosis trait when they have to terminally differentiate?

A

Nodules don’t just contain terminally differentiated bacterioids, they also have undifferentiated bacteria, thus increasing bacterial population
Differentiation of bacterioids is recent evolved trait imposed by legume to increase n fixing

47
Q

How do rhizobium mitotically activate the cortex cells?

A

Probably modulate phytohormine balance of cells (auxin:cytokinin ratio)

48
Q

What is the stele’s role in mitotic reactivation?

A

Nodule develops from cortex cells adjacent to protoxylem cells in the stele
These protoxylem cells may produce factor which functions in combo with rhizobia in reactivation

49
Q

How is the number of nodules regulated?

A

Tightly regulated
Too many results in parasitism not symbiosis
Systemic signal (unknown) moves through root system suppressing node formation
Hypernodulation mutants: excess number of nodules
Hyponodulation mutants: reduced number