Models for R-gene activation

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The guard hypothesis

A cellular complex of proteins, which includes both the 'guardee' molecule (red) and an NB-LRR protein (grey, shaded from the N terminus through NB and LRR domains), is a target for effector of disease (orange).Binding of the effector to its targets results in disassociation and activation of the NB-LRR protein and thus disease resistance. Alternatively, the NB-LRR protein may not be part of the target complex after effector binding. Recruitment to the effector/target complex would then activate the NB-LRR protein

The guard hypotesis.


The zig-zag model

The zig-zag model is a product of years of work by many labs attempts to synthesize PAMP perception, PTI, Effector/virulence factor function and NB-LRR based disese resistance. A brief description is reported below.

  • Phase 1: plants detect microbial/pathogen-associated molecular patterns (MAMPs/PAMPs, red diamonds) via PRRs to trigger PAMP-triggered immunity(PTI).
  • Phase 2: successful pathogens deliver effectors that interfere with PTI, or otherwise enable pathogen nutrition and dispersal, resulting in effector-triggered susceptibility (ETS).
  • Phase 3: one effector (indicated in red) is recognized by an NB-LRR protein, activating effector-triggered immunity (ETI), an amplified version of PTI that often passes a threshold for induction of hypersensitive cell death (HR).
  • Phase 4: pathogen isolates are selected that have lost the red effector, and perhaps gained new effectors through horizontal gene flow (in blue)—these can help pathogens to suppress ETI. Selection favours new plant NB-LRR alleles that can recognize one of the newly acquired effectors, resulting again in ETI.


The zig-zag model.


The switch model

In the absence of a pathogen, NB-LRR R proteins reside in an autoinhibited, ADP-bound "OFF" state that is stabilized by the LRR domain.. Effector-perception by the C-terminal part of the LRR domain changes the interface between its N-terminal part and the ARC2 subdomain, thereby creating a more open conformation of the R protein that is prone to nucleotide exchange. ADP/ATP exchange triggers a second conformational change, altering the interactions between the central NB-ARC, the N-terminal TIR/CC and C-terminal LRR domains resulting in the "ON" state. In the activated state, the NB subdomain becomes exposed to initiate defense signaling. ATP hydrolysis resets the protein into its ADP-bound autoinhibited "OFF" state.

The switch model.


The decoy model

Opposing selection forces are expected to operate on guarded effector targets in plants with or without the associated R protein. In the absence of the R protein targets will be under selective pressure to reduce the interaction and evade manipulation (left). In the presence of the R protein), the guarded effector target will be under selective pressure to improve the interaction with the effector and enhance pathogen perception. A gene duplication of the effector target or the independent evolution of a target mimic would reduce the evolutionary constraints imposed on the guarded effector target, allowing it to specialize as a coreceptor (decoy) that regulates the activation of the R protein.

The decoy model.
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