Common themes in plant pathogenesis: suppression of host defenses

1. Common themes in plant pathogenesis: suppression of host defenses • Successful pathogens overcome innate host defense responses by targeting receptors, signaling components, defense gene expression, or defense gene function. • Suppression of RNA silencing • Breaking through or breaking down physical or biochemical barriers • Suppression (or modulation) of basal defense (PTI) • Suppression (or modulation) of R gene–mediated HR or cell death (ETI)

2. Part II: overcoming plant defenses • Pectolytic enzymes in soft rot bacteria - redundancyHrp-dependent suppression of cell-wall based defenses • Type III effectors and defense • ETI vs. PTI • Effector targets in PTI and ETI • Early observations • A cool phenotype for assaying suppression of basal defense • Toxins and suppression of defense: the coronatine story revisited • Some interesting discoveries in fungi • Nematodes too • The (a) big picture • Discussion

3. Pectate WT pel- WT pel- pel- supnt. Chrys EXT Pectate Chrys EXT Kelemu, S., and Collmer, A. (1993). Erwinia chrysanthemi EC16 produces a second set of plant-inducible pectate lyase isozymes. Appl environ microbiol 59, 1756-1761.

4. Figure 2. Decoy model for plant resistance gene evolution. (a) The Pto kinase might have evolved to mimic the kinase domain of PRRs such as FLS2 and EFR, the intended targets for AvrPto. The Pto–AvrPto interaction triggers Prf-dependent ETI. (b) The Bs3 resistance gene might have evolved to mimic the promoter of upa20, a susceptibility gene targeted by AvrBs3. This leads to the specific expression of Bs3 and disease resistance in the presence of AvrBs3.

5. Figure 1. Host targets in bacterial virulence. The diagram depicts currently known host targets for plant pathogenic bacterial effectors (in orange). FLS2 and EFR are shown as representative surface-localized PRRs. SERKs are closely related to BAK1 and may similarly dimerize with PRRs upon ligand stimulation. RAR1, GRP7, and AtMIN7 regulate cell wall based defenses through unknown mechanisms. RAR1 negatively regulates flg22-induced callose deposition, whereas GRP7 positively regulates PAMP-induced callose. AtMIN7 may play a role in the ETI pathway (dashed line). AvrPto inhibits FLS2 and EFR to block the PTI pathway. HopAI1 irreversibly cleaves the C-OP bond to remove the phosphate group from phosphothreonine at the TXY motif and inactivates MAP kinases, thereby inhibiting PTI. HopU1 ribosylates GRP7 to inhibit PTI. AvrB interacts with RAR1 and presumably enhances the activity of RAR1 to inhibit PTI. AvrPtoB promotes the ubiquitination and degradation of Fen and prevents the initiation of Prf-mediated ETI. HopM1 destabilizes AtMIN7 to inhibit cell wall defenses. The AvrBs3/PthA family effectors directly bind plant promoter sequences and transcriptionally activate susceptibility gene expression.

6. Type III effectors suppress defense - early observations Brown et al. (1995) MPMI 8:825

7. Type III effectors and suppression of defense - early observations VirPphA mutant of P. syringae pv. phasolicola loses virulence and elicits weak HR (Jackson et al. 1999. PNAS) AvrPphC blocks HR elicited by AvrPphF. (AvrPphF blocks HR elicited by other Avr). These Rxs are cultivar-specific (Tsiamis et al. 2000. EMBO J.) WT cured PAI F WT cured F F+C S HR S S- S hr HR hr Canadian Wonder Tendergreen

8. Many effectors suppress HR and defense gene expression (e.g., Jamir et al. 2004. Plant J.) Weird effectors*… • HopPtoN • Suppresses HR, also limits death in disease (mutant causes more specks) • HopPtoM • Required for necrotic symptoms but not bacterial multiplication *Bring to mind viral silencing suppressor functions?

9. TECHNICAL ADVANCE: Oh, H.S., and Collmer, A. (2005) Basal resistance against bacteria in Nicotiana benthamiana leaves is accompanied by reduced vascular staining and suppressed by multiple Pseudomonas syringae type III secretion system effector proteins. Plant Journal44: 348-359.

10. Reduced vascular staining as indicator of basal resistance Functional assay for specific effectors Failure of challenge HR as indicator of basal resistance, and use as functional assay

11. Also good assays for elicitors of basal defense (PAMPS)

12. Not a type III effector! Melotto, M., Underwood, W., Koczan, J., Nomura, K., and He, S.Y. (2006) Plant stomata function iniInnate immunity against bacterial invasion. Cell 126, 969-80.

13. Some interesting discoveries of host defense suppression by phytopathogenic fungi Green islands occur in barley powdery mildew. P. infestans produces soluble glucans that suppress oxidative burst and HR in potato. M. pinodes produces glycopeptides that suppress phytoalexin production by pea and render it susceptible to avirulent Alternaria. S. lycopersici (leaf spot of tomato) detoxifies saponin. Saponin products inhibit HR. (two birds) Aggressive B. cinerea isolates inhibit secondary oxidative burst in bean suspension cells.

14. Unger, C., Kleta, S., Jandl, G., and von Tiedemann, A. (2005) Suppression of the defence-related oxidative burst in bean leaf tissue and bean suspension cells by the necrotrophic pathogen Botrytis cinerea. Journal of Phytopathology153: 15-26. 2-MS=2 methylsuccinate from culture supernatant of aggressive (virulent) isolate suppresses 2º oxidative burst induced by avirulent isolate

15. Nematodes Jammes, F., Lecomte, P., de Almeida-Engler, J., Bitton, F., Martin-Magniette, M.L., Renou, J.P., Abad, P., and Favery, B. (2005) Genome-wide expression profiling of the host response to root-knot nematode infection in Arabidopsis. Plant J44: 447-458.

16. da Cunha, L., McFall, A.J., and Mackey, D. (2006) Innate immunity in plants: a continuum of layered defenses. Microbes and Infection8: 1372-1381.

18. Discussion Basal defense prevents HR. Does that seem strange? Some effectors suppress HR and some induce it. Could there be selective advantage to maintain both? Why cause symptoms if you don’t have to?