Plant microbes exam Flashcards
Disease triangle
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.
Successful pathogen
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.
Bacterial PRR for flagellin
FLS2
Bacterial PRR for EF-Tu
EFR
Bacterial PRR for ax21
XA21
Bacterial PRR for peptidoglycans
LYM1, LYM3 and CERK1
Fungal PRR for xylanase
Eix1 and Eix2
Fungal PRR for Ave1
Ve1
Fungal PRR for chitin
CEBiP and CERK1
PRR (Pattern recognition Receptors)
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.
Phytoanticipins
Preformed antimicrobial compounds
Phytoalexins
Induced antimicrobial compounds. Altering phytoalexin production in plants can contribute to their defense, raise nutritional quality of foods and provide a source of medicines.
Camalexin
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
Bacteria effector secretion
Bacteria secrete their effectors via the type-III secretion system (T3SS) or other secretion systems. T3SS has a pilus that pierces the cell wall.
Fungi and oomycete effector secretion
Effectors are secreted from haustoria or tips of hyphae. Haustoria are specialised structures for nutrient uptake and effector delivery.
Nematode effector secretion
Secreted via their feeding stylet
Insect (phloem feeder) effector secretion
Secreted via stylets
Avr2 (Cladosporium fuluum (fungal))
Inhibits cyteine proteases in the apoplast (outside cells)
AvrPto (Pseudomonas syringae (bacteria))
Targets FLR2 (PRR) and interferes with signalling
Hop1 (Psudomonas syringae (bacteria))
Disrupts chloroplast structure and function
AvrBs3 (Xanthomonas campestris (bacteria))
Transcription activator-like (TAL) effector, turns on genes that favor pathogen survival.
PRR and R protein structure
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
Salicylic acid and Jasmonate
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.
Host-specific Necrotrophs
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.