Lect. 5 Host Pathogen interaction-II

Host-Pathogen
interaction-II
Pl Path 604
PN Sharma
Department of Plant Pathology
CSK HPKV, Palampur-176062

• It was originally believed that gene-for-gene resistance
was conferred by a direct interaction between the R
gene product and the Avr gene product, but
experiments failed to show this.
• Lack of evidence for a direct interaction indicated the
involvement of some other type of interaction between
the R gene and Avr gene products and this lead to the
concept of indirect interaction models leading to
resistance.

GUARD HYPOTHESIS
Vander Biezen and Jones, 1998
• lack of evidence for a direct interaction
indicated the involvement of some other type
of interaction between the R gene and Avr
gene products and led to the formation of the
guard hypothesis.
• This model proposes that the R proteins
interact, or guard, a protein known as the
guardee, which is the target of the Avr protein.
When it detects interference with the guardee
protein, it activates resistance.

Guard Hypothesis
1. (A) A cellular complex of
proteins (blue), which includes
both the ‘guardee’ molecule
(red) and a resistance gene
2. (B) Binding of the effector to
its target results in dissociation
and activation of R-gene and
thus disease resistance.
3. (C) Alternatively, the R-gene
may not be part of the target
complex until effector binding.
4. (D) Recruitment to the
effector/target complex would
then activate the R-gene.

Elicitor
Target
R-gene
(Vander Biezen and Jones, 1998. Current Biology)

Support of guard model
• No direct interaction is found between Ave
factor and R proteins except shown in Avr ptopto
and Avr pita-pita
• Recognition of the Avr factor requires an
additional host protein that is specific for each
Ave-R pairs.
• Structure of predicted function of this host
protein, or its general occurrence, suggest that
it might be a virulence target for the pathogen.

DIFFERENT INDIRECT MODELS TO
SUPPORT GUARD HYPOTHESIS
• Bridge : Effector binds independency to the
R-protein into G the third protein, recruiting
one to the other. The effector dependent
interaction of these two proteins activates
downstream signalling for defense.

R- protein
Avr
RESISTANCE
Target
protein
(Source Martin et al., 2003. Annual Review of Plant Biology)

2. Matchmaker :
• Effector induces a direct interaction
between R protein and a third protein by
causing a conformational change in one or
the other. The effector may or may not
remains associated with the complex
following binding CA two plant protein.

R
Avr
OR
RESISTANCE
Target protein
(Source Martin et al., 2003. Annual Review of Plant Biology)

Affinity enhancement :
• Interaction of the effector with the R-prtein a
third protein or both, stabilizes a pre-existing,
work interaction between the NO plant
proteins such that abundance of the complex
increase to drives dream signalling to activate
the induced defense in steady state levels of
interaction between the two plant proteins
function to maintain basal defense.

Avr
R
OR
RESISTANCE
(Source Martin et al., 2003. Annual Review of Plant Biology)

De-repression :
• Effector derepresser defense responses by
disrupting an interaction of the R protein and a
third protein that negatively regulates activity
of the R protein.

Avr
R
Target protein
And/ or
RESISTANCE
(Source Martin et al., 2003. Annual Review of Plant Biology)

Dual recognition
• This model in which independent interactioins
between the effector to the R gene and the
effector a third protein are both required for
resistance.

R
Avr
And
RESISTANCE
Target protein
(Source Martin et al., 2003. Annual Review of Plant Biology)

RECENT EXAMPLES OF PLANT-PATHOGEN
INTERACTIONS SUPPORTING GUARD HYPOTHESIS
a. Arabidopsis RPM1 is a peripheral plasma membrane NB-
LRR protein. It is activated by either the AvrRpm1 or the
AvrB effector proteins. AvrRpm1 enhances the virulence
of some P. syringae strains on Arabidopsis as does AvrB
on soybeans. AvrRpm1 and AvrB are modified by
eukaryote-specific acylation once delivered into the cell
by the type III secretion system (red syringe) and are thus
targeted to the plasma membrane. The biochemical
functions of AvrRpm1 and AvrB are unknown, although
they target RIN4, which becomes phosphorylated (1P),
and activate RPM1. In the absence of RPM1, AvrRpm1
and AvrB presumably act on RIN4 and other targets to
contribute to virulence. Light blue eggs in this and
subsequent panels represent as yet unknown proteins.

Arabidopsis-P. syringae system
( Source: Jones and dangl, 2006. Nature)

. RPS2 is an NB-LRR protein that resides at the
plasma membrane. It is activated by the AvrRpt2
cysteine protease type III effector from P.
syringae. Auto-processing of AvrRpt2 by a host
cyclophilin reveals a consensus, but
unconfirmed, myristoylation site at the new
amino terminus, suggesting that it might also be
localized to the host plasma membrane. AvrRpt2
is the third effector that targets RIN4. Cleavage
of RIN4 by AvrRpt2 leads to RPS2-mediated
ETI. In the absence of RPS2, AvrRpt2
presumably cleaves RIN4 and other targets as
part of its virulence function.

C. RPS5 is an Arabidopsis NB-LRR protein localized
to a membrane fraction, probably via acylation.
RPS5 is NDR1-independent. It is activated by the
AvrPphB cysteine protease effector from P.
syringae. AvrPphB is cleaved, acylated and
delivered to the host plasma membrane. Activated
AvrPphB cleaves the Arabidopsis PBS1 serinethreonine
protein kinase, leading to RPS5
activation. The catalytic activity of cleaved PBS1 is
required for RPS5 activation, suggesting that this
‘modified-self’ fragment retains its enzymatic
activity as part of the RPS5 activation mechanism.
To date, no function has been ascribed to PBS1 in
the absence of RPS5.

Arabidopsis-P. syringae system
B. RPS2 is an NB-LRR protein that resides at the plasma
membrane. It is activated by the AvrRpt2 cysteine
protease type III effector from P. syringae. Autoprocessing
of AvrRpt2 by a host cyclophilin reveals a
consensus, but unconfirmed, myristoylation site at the
new amino terminus, suggesting that it might also be
localized to the host plasma membrane. AvrRpt2 is the
third effector that targets RIN4. Cleavage of RIN4 by
AvrRpt2 leads to RPS2-mediated ETI. In the absence
of RPS2, AvrRpt2 presumably cleaves RIN4 and other
targets as part of its virulence function.

D. Pto is a tomato serinethreonine protein kinase.
Pto is polymorphic and hence satisfies the genetic
criteria for the definition of a disease resistance
protein. Pto activity requires the NB-LRR protein
Prf, and the proteins form a molecular complex.
Prf is monomorphic, at least in the tomato species
analysed to date. Pto is the direct target of two
unrelated P. syringae effectors, AvrPto and
AvrPtoB, each of which contributes to pathogen
virulence in pto mutants. It is thus likely that Prf
guards Pto. The Pto kinase is apparently not
required for PTI, though there may be
redundancy in its function because it is a member
of a gene family.

Contd…
Arabidopsis-P. syringae system
(Source Jones and dangl, 2006)

Tomato – P. syringae system

E. The transmembrane RLP Cf-2 guards the
extracellular cysteine protease Rcr3. Cf-2
recognizes the C. fulvum extracellular
effector Avr2, which encodes a cysteine
protease inhibitor. Avr2 binds and inhibits
the tomato Rcr3 cysteine protease.
Mutations in Rcr3 result in the specific loss
of Cf-2-dependent recognition of Avr2.
Hence, Cf-2 seems to monitor the state of
Rcr3, and activates defence if Rcr3 is
inhibited by Avr2.

Tomato- C. Fulvum system
Contd…
(Source: Jones and dangl, 2006)