Lecture 3 - plant pathogens Flashcards

1
Q

What is the importance of plants?

A

Plants are vital for-
atmospheric oxygen
food
environment/wildlife
carbon storage (50% of dry mass of a tree is carbon)
Also useful for
textiles
(bio)fuels
medicines incl. anti-microbials
vaccines

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2
Q

what are the impacts of plant pathogens?

A

many different pathogens – >20,000 fungi, >4100 nematodes, ~1,000 viruses, ~200 bacteria & 100s of protist parasites

Food & Agricultural Organisation of the United Nations (FAO) estimates
plant pathogens cost global economy US$220 billion/year
20-40% crops lost to pests

threaten food security & livelihoods
loss of plant species & dependent organisms
changes to countryside
climate change likely to increase spread & change distribution of plant pathogens & pests
see Singh et al., 2023 Nat Rev Microbiol 21: 640-656 if interested – OPTIONAL!
costs of mitigation strategies

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3
Q

what are types of plant pathogens?

A

Necrosis-
death of cells
spots and rot on leaves

Soft rot-
enzymatic degradation of plant tissues

Wilt-
loss of turgor in leaves

Blight-
discolouration, wilting and death of foliage

Cankers-
dead sections of bark

Gall-
tumourous growth

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4
Q

what is the great Irish potato famine?

A

Mass starvation in Europe in 1840s following successive epidemics of potato late blight
100,000 deaths
caused by Phytophthora infestans

Great Irish Potato Famine 1845-1855
poor farmers gave cereals to English landlords, so diet was almost entirely potatoes
few varieties grown, all sensitive to blight
up to 1 million people died, and 2 million emigrated to Australia and N. America
many more evicted from farms as access to workhouse aid forbidden if had >¼ acre land

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5
Q

what is potato late blight?

A

Devastating plant disease even today
Potatoes = 4th largest food crop
$6.7 billion losses annually due to blight
Caused by Phytophthora infestans
Oomycete (protist) related to brown algae & diatoms
Synthesises cellulose cell walls
exert pressure & destroy host cells
Dispersed by sporangia

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6
Q

how do you control potato blight?

A

Highly challenging as P. infestans rapidly adapts to control measures
huge, highly repetitive genome (240 Mb)
effector genes important for infection show rapid expansion & turnover

Intensive use of fungicides
Destroying foliage before lifting potatoes
Breed resistant cultivars
introduce Rpi resistance genes from wild potato species into agricultural lines
lengthy & complicated process
CRISPR/Cas9 technology may help

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7
Q

what is fusarium tilt of the banana?

A

Bananas are globally most traded fruit
>400 million people rely on bananas & plantain for food security & income
155 million tonnes produced annually
Fusarium oxysporum fungus causes banana wilt (or Panama disease)
Gros Michel banana variety highly susceptible to F. oxysporum Tropical Race 1 (TR1) – severe losses in Latin America prior to 1960s
replaced with Cavendish variety, which is now threatened by TR4 Fusarium

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8
Q

how do we control fusarium wilt?

A

hard to eradicate
persists in soil & infects via roots
symptoms take time to appear after infection
commercial monoculture means few options to find resistant strains

prior exposure to avirulent TR1 strain from Brazil can offer temporary protection from TR4
can the protective mechanisms be harnessed to protect longer term?

multi-site fungicides also being developed

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9
Q

what is dutch elm disease?

A

Caused by fungi Ophiostoma ulmi and O. novo-ulmi

Discovered & isolated in Holland in 1921 by Marie Beatrice Schwarz

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10
Q

how is dutch elm disease spread?

A

By elm bark beetle
Root grafts
Infected logs

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11
Q

what is pathogenesis?

A

Fungus blocks water conduction channels (xylem) causing wilt
polysaccharides & glycoproteins
host defence response also plugs vessels

Shoots die back from tip – shepherd’s crook
Cell wall degrading enzymes help fungus invade the xylem

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12
Q

what is the significance of dutch elm disease?

A

First appeared in NW Europe in 1910
O. ulmi

Epidemic died down in 1940s, having killed 10-40% elms in different European countries

2nd outbreak in late 1960s
highly aggressive O. novo-ulmi

Accidently introduced into England from Canada in 1960s
most mature English elms died by early 1980s (>60 million)
spread to Scotland within 10 yrs (movement of elm products)
today, only ~1000 mature elms in UK remain outside cordons in Brighton & Edinburgh

As young seedlings grow large enough to support beetle breeding, DED is now returning

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13
Q

what is the control of dutch elm disease?

A

Early reporting & action
Reduce elm bark beetle population
insecticides
remove damaged bark/branches
removal of elm firewood piles
Prevent/destroy root grafting
Prune only when bark beetle dormant
Fungicides
Topical or by injection
Can’t eliminate once infection started

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14
Q

what is chalara ash dieback disease?

A

Caused by wind-borne fungal pathogen Hymenoscyphus fraxineus (previously Chalara fraxinea)
First detected in UK in 2012

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15
Q

what are the challenges for phytopathogens?

A

Vary greatly in temperature

Very basic transport/communication system
inefficient transport of microbes within plant

Surface microbes
exposed to oxygen
rich in organic matter
exposed to light and UV irradiation

Root microbes
less variable environment
high nutrient levels

Vulnerable to extremes of weather

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16
Q

how does chalara ash back spread?

A

Waxy coatings on leaves and stems
bacteria gain access through gas or water pores or enter via wounds and multiply in intercellular spaces
nematodes feed by inserting stylet into cells
fungi use hyphae to invade between cells and specialised hyphae form haustoria to enter cells

17
Q

what is the plant immune response?

A

1) Pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI)
general immune response that works against many pathogens, but fairly weak

2) Effector-triggered immunity (ETI)
stronger immune response to specific pathogen, which can lead to longer-term systemic acquired resistance (SAR)

in-built tolerance to some microbes e.g. Mycorrhizae
all cells capable of mounting immune response

18
Q

what is pamp triggered immunity?

A

PAMPs e.g. bacterial flagellin, LPS, peptidoglycan, fungal chitin are recognised by plant pattern recognition receptors (PRRs)

PRRs are transmembrane proteins with extracellular ligand-binding domain & intracellular kinase domain

Results in production of host defensive molecules to impede pathogen advance

Some pathogens produce avirulence (Avr) effector proteins to avoid PTI

19
Q

what is effector triggered immunity?

A

Plant resistance (R) protein receptors e.g. NLRs (intracellular nucleotide-binding domains & leucine-rich repeat proteins) recognise pathogen effector molecules leading to a stronger ETI response

Plant resistance proteins can also trigger ETI by sensing damaged plant molecules (damage-associated molecular patterns or DAMPs)

triggers Ca2+ signalling, reactive oxygen species (ROS), accumulation of pathogenesis-related proteins e.g. phytoalexins

may activate hypersensitive response (programmed cell death at infection site)

changes in plant hormone levels (salicyclic acid & jasmonic acid) may lead to SAR (systemic acquired resistance)

20
Q

what are the results of pathogen detection?

A

-Cell wall modification
-thickens with added defensive compounds
-more resistant to turgor pressure/hydrolytic enzymes
-Closure of stomata
-Production of ROS
-Hypersensitive response
-Production of anti-parasite compounds & proteins
-phytoalexins, chitinases, defensins, protease inhibitors

21
Q

how do we manage plant pathogens?

A

Avoidance
where, when, how you plant, quarantining, crop rotation

Therapy
fungicides/antibiotics

Eradication
heat/fumigation of bulbs/seed/soil etc
cut off affected part of plant (no mobile immune cells & underdeveloped circulatory system)
destroy diseased plant material

Breeding resistant/genetically modified plants

Biocontrol e.g. bacteria & fungi as antagonists

22
Q

triangle of pseudomonas spp

A

P. aeruginosa-
human & plant pathogen
nosocomial pathogen (cystic fibrosis, immunosuppressed)
sepsis (burns patients)
soft rot in Arabidopsis & lettuce
forms biofilms
intrinsic antibiotic resistance
bioremediation
plant infection model for human disease

P. fluorescens-
plant commensal
biocontrol agent
lethal to mosquitoes & their larvae
acquires iron (siderophores) & tolerates stress
produces antibiotics

P. syringae-
causes disease in wide range of crops
seed borne & spread by rain
bacterial speck (tomatoes)
stunts growth
frost damage
nucleates snow & catalyses ice formation
artificial snow

22
Q

are some plant pathogens useful?

A

yes, they can be exploited for industry, genetic modification & biotechnology

23
Q

what is Agrobacterium tumefaciens

A

Bacterium causing crown gall disease

Independently replicating Tumour induction (Ti) plasmid integrates into plant genome.

24
Q

what is the Exploitation of A. tumefaciens?

A

Tumour genes in Ti plasmid can be disarmed

Recombinant proteins can be inserted, resulting in transgenic plant

Disease resistant plants

Production of pharmaceuticals

25
Q

what isTobacco mosaic virus (TMV)?

A

First virus to be discovered (1892)
Affects tobacco, peppers & tomatoes
1940s, 2-3% tobacco crop lost to TMV

Easily purified RNA virus
encoding 2 replicases, movement protein & coat protein

Coat protein replaced by gene of interest to express/produce transproteins
cholera toxin B subunit for vaccine
antibodies
biosensor enzymes e.g. penicillinase, horseradish peroxidase

Forms viral nanoparticles
genetically modify TMV to display vaccine epitope eg malaria, non-Hodgkin’s lymphoma
chemically conjugate to use as drug delivery system or to carry fluorescent molecules for medical imaging

Transgenic plants expressing TMV components display resistance to TMV & related plant viruses