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

Transcription

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

2 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.

3 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.

4 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.

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

6 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.

7 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.

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

9 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.

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

11 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.

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

13 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.

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

15 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.

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

17 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.

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

19 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. 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.

20 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.

21 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.

22 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.

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

24 Tomato P. syringae system

25 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.

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