Plant microbes exam Flashcards

1
Q

Disease triangle

A

Defines what makes a microbe interaction a disease. Pathogen – overcomes plant defence. Host – must be susceptible to the pathogen. Environment – must tip the balance in favor of the pathogen.

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2
Q

Successful pathogen

A

Pathogenesis genes and effectors allow the pathogen to enter into the plant, evade defenses, survive and reproduce. An increased number of pathogens leads to an increased chance of success. Must be able to find the host and attach, they can use stomata to enter, and puncture cell walls. Enter past the plants impermeable defenses. Avoid defense. Grow and reproduce and spread.

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3
Q

Bacterial PRR for flagellin

A

FLS2

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4
Q

Bacterial PRR for EF-Tu

A

EFR

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5
Q

Bacterial PRR for ax21

A

XA21

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6
Q

Bacterial PRR for peptidoglycans

A

LYM1, LYM3 and CERK1

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7
Q

Fungal PRR for xylanase

A

Eix1 and Eix2

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8
Q

Fungal PRR for Ave1

A

Ve1

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9
Q

Fungal PRR for chitin

A

CEBiP and CERK1

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10
Q

PRR (Pattern recognition Receptors)

A

The PAMP is recognised by the external leucine rich repeat domain of the PRR protein kinase which triggers the activation of a protein kinase signalling cascade, a NADPH oxidase and a calcium. NADPH oxidase enzyme catalyzes the production of super oxide (O2-) which is converted to hydrogen peroxidase (H2O2). The increased calcium and H2O2 and the activated protein kinase domain activate a protein kinase signalling cascade that results in the activation of defense response.

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11
Q

Phytoanticipins

A

Preformed antimicrobial compounds

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12
Q

Phytoalexins

A

Induced antimicrobial compounds. Altering phytoalexin production in plants can contribute to their defense, raise nutritional quality of foods and provide a source of medicines.

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13
Q

Camalexin

A

Arabidopsis phytoalexin. Show it to be induced by a variety of pathways. Some studies show JA signalling has control of its synthesis. Some studies suggest SA dependent and independent pathways control synthesis. Ethylene signalling might be induced. Some suggest H2O2 and SA are needed to induce synthesis. Possibly causes membrane damage

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14
Q

Bacteria effector secretion

A

Bacteria secrete their effectors via the type-III secretion system (T3SS) or other secretion systems. T3SS has a pilus that pierces the cell wall.

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15
Q

Fungi and oomycete effector secretion

A

Effectors are secreted from haustoria or tips of hyphae. Haustoria are specialised structures for nutrient uptake and effector delivery.

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16
Q

Nematode effector secretion

A

Secreted via their feeding stylet

17
Q

Insect (phloem feeder) effector secretion

A

Secreted via stylets

18
Q

Avr2 (Cladosporium fuluum (fungal))

A

Inhibits cyteine proteases in the apoplast (outside cells)

19
Q

AvrPto (Pseudomonas syringae (bacteria))

A

Targets FLR2 (PRR) and interferes with signalling

20
Q

Hop1 (Psudomonas syringae (bacteria))

A

Disrupts chloroplast structure and function

21
Q

AvrBs3 (Xanthomonas campestris (bacteria))

A

Transcription activator-like (TAL) effector, turns on genes that favor pathogen survival.

22
Q

PRR and R protein structure

A

Domains of R protein: NBS = Nucleotide binding site. LRR = Leucine rich repeat, confers specificity to the binding interaction. TIR = Toll interleukin receptor. CC = coiled cloil.
Domains of PRR: LRR = Leucine rich repeat. TM = transmembrane.
PRR = LRR – TM – Kinase
R protein 1 = TIR – NBS – LRR
R protein 2 = CC – NBS – LRR

23
Q

Salicylic acid and Jasmonate

A

There are phytohormones that differentially contribute to defenses against biotrophs and necrotrophs. Upon the recognition of a microbial molecule, immune receptors can activate phytohormone signalling pathways. SA and JA often work antagonistically, but sometimes work synergistically. Pathogens often exploit their antagonistic interactions to promote virulence. SA usually triggers resistance against biotrophs and hemibiotrophs.

24
Q

Host-specific Necrotrophs

A

Produce specific toxins that are necessary for their pathogenicity. Sometimes these act through specific R genes in a counter intuative manner. By being detected by R proteins they can activate cell death. The necrotroph secretes host selective toxins, the plant cell can detoxify some toxins and activate toxin triggered immunity (TTI). Some proteins bind virulence targets that get recongised by R proteins, this triggers Necrosis.

25
Q

Broad host range necrotrophs

A

Produce cell wall degrading enzymes (CWDEs), necrosis and ethylene inducing proteins (NEPs) and can suppress the plants immune response. Plants can detect damaged cell walls to activate immunity. DAMPs = Damage associated molecilar patterns. PAMPs and DAMPs trigger immune response. Toxins, CWDEs, NEPS and oxalic acid may trigger some immunity, but mostly manage to suppress it.

26
Q

Phytophthora infestans

A

Hemibiotroph. It first invades the plant via appressoria and intercellular haustoria. Eventually they can cause necrosis in plant tissue and form spores to infect other plants. They start as zoospores which then form appressorium and grow between cells, where they can form haustorium.

Switching form biotroph to Necrotroph.
Initiallty the P. infestans effectors suppress defense response, but later they produce necrosis inducing effectors. Initially they secrete SNE1 (effectors) which blocks programmed cell death and plant defense response that are normally induced by R genes and NLPs. This produces no symptoms of infections. Once the apthogen has excessively proliferated through the host tissue, secreted proteins such as NLPs induces rapid cell death and necrosis.

27
Q

Pathogens needs to be able to penetrate or circumvent physical barriers

A

Some produce a melanised appressoria, which builds up high pressure to puncture the cell wall.
Some pathogens enter via the stomata and grow extracellularly.
Some pathogens produce non-melanised, but effective appressoria.

28
Q

Pathogen host attachment

A

Some pathogens use extracellular polysaccharides to attach to hosts.
Biofilms are formed by bacterial communities that form a cluster in which the cells are embedded with a matrix of extracellular polymeric compounds attached to a surface. Some form polysaccharides to stick and form biofilms in the xylem.
Magnaporthe grisea – causal agent for rice blast. Produces extracellular hydrophobin proteins required for adhesion and penetration. Deficient mutants are less pathogenic.

29
Q

siRNAs – Plant virus response

A

This includes RNA-mediated silencing and hypersensitive response. Viral RNA is replicated to form dsRNA via RDRs (RNA dependent RNA polymerase). Viral dsRNA can be cleaved by DCLs, DCL2 and DCL4. This produces short interfering RNAs (siRNAs) which bind to the risc complex and direct the cleavage of viral RNA.

30
Q

Virus Immune response

A

Viruses enter a cell through wounding, introduced by an insect or they can enter via cell-to-cell transfer as virions or viral ribonucleoproteins (vRNPs). Within a cell, a virus is disassembled, viral proteins are made, the viral genome is replicated and encapsilated as new viral particles (virions/vRNPs). Viral components can trigger immune responses through PRRs and R proteins, leading to cell death and systemic immunity.

31
Q

Nitrogenase

A

Ferredoxin(red) reduces Fe(ox), producing Fe(red). Fe(red) then reduces MoFe(ox) to produce MoFe(red). MoFe(red) reduces N2 to produce 2 ammonia (NH3). Fe(ox) requires 16 ATP to regenerate into Fe(red). Overall it takes 8 protons and N2, with 16 ATP to produce 2 NH3.

32
Q

Macronutrients

A

Their concentration in plant dry material is about 1000-1500 ug/g. These include nitrogen, phosphorous, calcium, magnesium, potassium, sulphur. A high amount of these is needed.

33
Q

Micronutrients

A

Their concentration in plant dry material is about 0.005-100 ug/g. These include Chlorine, boron, iron, Manganese, Zinc, Copper, Molybdenum, Nickel

34
Q

Magnesium

A

Essential for confromational satbilisation of macromolecules such as nucleic acids, proteins, cell membranes and walls. Maintin the enzymatic activities of proton ATPases, dinases and polymerase. Regulator of cation-anion balance in cells and osmotically active ions in regulating cell turgor. Associated with chlorophyll, essential for photosynthesis.

35
Q

Chlorine

A

Regulate turgor in stomata guard cells, involved in O2 production.

36
Q

Boron

A

Important for sugar translocation and carb metabolism. Needed in cell division, important for flowering, pollen tube growth, frutiing, N metabolism,

37
Q

Flavenoids

A

Flavenoids are shown to stimulate or inhibit the rhizobia nod gene expression and cause chemoattraction of rhizobia to the root. Flavenoid detection initiates host specific chemotaxis and induces expression of nod genes.

38
Q
A