22. Plant bacteria Flashcards

1
Q

What is a rough template for bacterial infection?

1

A
  1. Dissemination through water, seeds and invertebrates
  2. Entry through wounds or natural openings
  3. Suppression of host defences using intracellular/extracellular effectors, toxins and hormones
  4. Modulation of host physiology
  5. Generation of environment conducive to bacterial growth
  6. Protection from environmental stress
  7. Host specificity
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2
Q

What bacterial systems are discussed in this lecture?

2

A
  1. Foliar endophytes
  2. Vascular wilts
  3. Soft rots
  4. Galls and hairy roots
  5. Developmental dystrophies
  6. Case study: Xylella
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3
Q

Describe foliar endophytes

3

A

Pseudomonas syringae

Symptoms: Only occur when bacteria reach high densities. Can lead to chlorosis, canker, then cell death due to toxins, apoptosis and necrosis

Lifecycle: Transmitted in many ways - making it an ideal pathogen in many ways. Spreads through the water cycle, insects and the seeds/germplasm

Challenges for pathogen entry: Requires water, and stomata to entry. Bacterial toxins like coronatine (COR) can be used to facilitate stomatal opening, and then close them to maintain humidity

Bacterial attack on plants: (1) Release of the Ice nucleaton protein, InaZ, which promotes ice crystal formation, (2) Production of Extracellular Polysaccharides (EPS) to promote adhesion and stress tolerance, (3) T3SS, which delivers proteins that help to create environment more conducive to bacterial growth, and suppresses PTI

Plant immunity: Recognises PAMP molecules, which the T3SS suppresses

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4
Q

Describe vascular wilts

4

A

Ralstonia spp.

Life cycle: Characterised by the invasion and blocking of the xylem. Involves a phenotypic switch to produce EPS once the quorum sensing threshold has been reached

Phase I: Suppression of host defences, and niche establishment using protein effectors and host molecules. T3SS is important for suppressing host defences in the root.

Phase II: Multiplication in the xylem, blockage of xylem vessels, movement rhgouth the xylem using cell wall degrading enzymes. Clogging of the xylem via bacteria and EPS

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5
Q

Describe galls and hairy roots

6

A

Phytoplasma

Life cycle: Dissemination by insect vectors, and the parasitic plant dodder. Mostly spread by phloem-feeding vectors

Symptoms: ‘Witches-broom’, which is the clustering of branches, virescence (which is the green coloration of non-green parts), bolting (growth of elongated stalks), formation of bunchy, fibrous secondary roots, reddening of leaves and stems

Economic uses: Ornamental Poinsettias.

Modulation of host phenotype: The use of Sec-dependent protein secretion systems. Means that just one protein can give a vast array of symptoms and effects. One example is SAP05, which is one of the 56 candidate effectors secreted by Aster Yellow Witches’ Broom, which directs plant transcription factors like GATA and SPL to the proteasome and change growth patterns

Symptoms and survival: Phytoplasma changes the growth patterns of young leaves in plants, which may make them more attractive to insect vectors, and increase their own survival

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6
Q

Describe soft rot

5

A

Pectobacterium spp.
Dickeya spp.

Life cycle: Characterised by the invasion and blocking of the xylem. Bacteria from an infected seed spread via invertebrates/soil to neighbouring plants. In the summer, the contaminated plants develop soft rot and develop in intracellular spaces

Phase I: Suppression of host defences using effectors and small molecules and/or T3SS, which secretes effectors. Production of an ‘arsenal’ of degrading enzymes that break down cell wall

Phase II: Degradation of cell walls and killing of host cells, controlled by quorum sensing. After reaching critical mass, signalling molecules are high, and indicate to produce cell wall degrading enzymes, like NLPs

Plant immunity: Plants can detect cell wall degradation via the DAMPs that are produced

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7
Q

Drescribe Xylella

7

A

History: Has been infecting olive plants since 2013, and has spread out from Puglia. There has been much objection to containment measures, and much public suspicion of scientists.

Current status: Can infect over 350 woody and herbaceous hosts, and is highly economically dangerous

Lifecycle: Remains located in the xylem, and varies the genes that it produces to induce EPS, and degrade the xylem vvessels. Causes significant issues for water transport. Has quorum-sensing mechanisms that it uses to decide what stage of life cycle to enter

Mechanism of damage: Production of cell-wall degrading enzymes

Fighting: (1) Detection, and the eradiation of infected plants, (2) Blocking the imports of infected plants, (3) Antimicrobials and biofilms, (4) Vector control

Are control measures environmentally damaging…?

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