TECHNICAL UNIVERSITY OF MOMBASA

DEPARTMENT OF PURE AND APPLIED

SCIENCES
MASTERS OF SCIENCE IN BIOCHEMISTRY
BENARD APIRI
MBC/0005/2022
UNIT NAME: BIOSIGNALLING
UNIT CODE: ABT 5104
SUBMITTED TO: DR.KIBITI
SUBMITTTED ON: 13TH JULY 2022
TASK: ASSIGNMENT 1
The guard hypothesis as a conceptual framework for the action of disease
effectors and the R-protein complex .Discuss.
The ‘guard hypothesis’ gives a conspiring conceptual framework for the action of disease
effectors and the R-protein complex. It aims at justifying to why Pto protein kinase needs the
NB- LRR protein Prf to start up defence just after the recognition of AvrPto. In accordance to
this model, Pto is a common unit of host defense, conceivably in a pathway for response to
nonspecific elicitors of phytopathogenic bacteria. AvrPto for P. syringae targets Pto and triumph
over nonspecific defense pathway hence Prf an NB-LRR protein that ‘guards’ Pto, ascertains its
prologue by AvrPto which is then followed by starting off of defense.
In this model, R proteins physically interact with cellular targets of bacterial type III effectors of
disease. The targets include either components of plant defense or proteins of the host whose
workability has been altered to maintain extracellular bacterial colony. In a general sense, type
III effectors gets into the resistant host cell, and associates with a target, leading to a complex
that is recognized by the R protein that is in turn induces disease resistance. When a specific R
protein not present, the host target open to virulence function of the type III effectors, and
disease ensues. In one deterministic scheme, R protein attaches to its guardee imminently, but
detach just after the type III effectors attaches to the guardee, leading to a functional R protein.
This is in harmony with the extermination that over expression of Prf results to imminent disease
resistance. This model proposes that NB-LRR proteins, and the signaling pathways arbitrates, are
negatively controlled by their own guardees.
On the other hand, R-protein conscription can be controlled by association of the type III effectors
with its cellular target protein. A conformational alteration that follows would then result to
increased affinity of the guardee–effector complex for the R protein, activating resistance. The
two models are compatible with the overall lack of direct interaction among NB-LRR proteins
and Avr proteins. Each plot is in harmony with the ideal framework that R proteins oversee if a
cellular protein is undergoing any attacks from effectors protein of the pathogen. The guard
hypothesis has quite a number of hypotheses:
I. R proteins can associate constitutionally with their ‘guardees’. Such associators will be
targets of virulence factors needed for a victorious infection, and/or constituents of
defense signaling. These potentiality isn’t reciprocally exclusive if the formal target of
virulence has also made progress, a function in the steadiness of an R-containing complex
whose structural integrity is needed for resistance.
II. The complex of the effectors with its target might be present in both susceptible and
resistant host cells, except that in the latter the R protein will also be part of the complex.
This suggests that a mutation in an R-protein partner might result in a loss of resistance
conferred by that R protein.
III. Multiple R proteins could physically associate with the same host protein complex and
hence with each other. When a slight number of host protein complexes are targets of the
effectors set from a given pathogen, then one host protein complex may be a target for
many pathogen effectors molecules. This can describe functional interference of two
structurally related R proteins.
IV. A culmination of this prognostication is that the number host’s cellular targets of type III
effectors might indeed be small and possibly aimed by quite a number of effectors. This is
evident as in two examples of a single R protein that can identify two effectors that are
different
 Representation of the guard hypothesis for R-protein function
a-cellular complex of proteins that has guardee molecule and NB-LRR protein .
b-Binding of the type III effector to its targets leading to detaching and turn on of NB-LRR proteins
and thus resistance.
c-NB-LRR protein may not be part of the target until after type III effector binding.
d-recruitment to the type III effector complex that activates the NL-LRR