EG 5&6 Flashcards
what are effectors
pathogen adaptation that is secreted or injected into host to improve virulence of a pathogen
what was plants response to evolution of effectors
plants evolved mechanisms to sense effectors through detecting the presence of R proteins (NLRs), this detection triggers an ETI response
what is the gene for gene model
-proposed by Harold Henry Flor in 1930/40s experimenting on flax rust
-model states that: a plant is resistant to a pathogen when it has a dominant allele of a Resistance gene (R-gene) whose product can recognise specifically a pathogen avirulence factor (a pathogen effector)
what are R proteins (NLRs) composed of
leucine rich repeat (LRR) which binds the effector or another plant protein, and a nucleotide-binding site (NBS) which binds ATP (active NLR) or ADP (inactive NLR)
what are the 2 sub families of NLRs and what defines them
the N terminal domain defines them, Toll Interleukin Receptor (TIR) and Coiled Coil (CC)
how do NLRs recognise effectors directly
differences in the amino acid sequences of the LRR domain of different NLR proteins gives them the ability to recognise different effectors which are bound by the LRR domain, rare
how do NLRs recognise effectors indirectly
-the effector modifies a target plant protein (not an NLR) increasing virulence of the pathogen, the same protein may be the target of multiple effectors each from its own pathogen
-NLR detects the modification of this protein
-effector target proteins are ‘guarded’ by NLRs through monitoring of any alterations, 1 target protein can be guarded by multiple NLRs
-2 methods: guard model and decoy model
what is an effector called following recognition
once an effector is recognised by an NLR and an ETI is triggered the effector is then known as an avirulence factor
what is the guard hypothesis
the guardee is the host protein that can be modified by the effector which is then detected by an NLR, host protein is ‘guarded’ by an NLR
ETI signalling pathways
ETI is very similar to PTI using mostly the same signalling pathways, hormones, genes etc. but ETI is a longer, stronger, and quicker response than PTI
what is hypersensitive response (HR)
HR or hypersensitive cell death response occurs in regions of high SA levels surrounding a point of infection
what is an example of NLRs (R proteins) recognising effectors
RIN4 and RPM1/RPS2, RIN4 is modified by effectors from Pseudomonas syringae, RIN4 is considered a negative regulator of the 2 proteins named above
what is effective resistance
minimum response required to overcome a pathogen, PTI related
what is the threshold for HR
higher level of immunity/defence corresponds to hypersensitive response, ETI related
what is effector triggered susceptibility (ETS)
presence of effectors reduces the defence response below the minimum threshold for effective resistance, no R protein to detect effector
