Resistance to Bacterial Pathogens in Plants

Abstract

To successfully infect a plant, pathogens must overcome three layers of defense: (1) preformed physical barriers; (2) a cell‐surface‐based surveillance system that detects conserved pathogen molecules and (3) an intracellular surveillance system that detects effector proteins injected into host cells. Bacterial plant pathogens overcome the first layer either by invading through natural openings and wounds, and/or by secreting hydrolytic enzymes that break down surface layers. Bacteria typically overcome the second layer by injecting effectors that interfere with defense signaling. Bacteria overcome the third layer either by modifying or eliminating existing effectors, or by evolving new effectors that suppress defense activation.

Keywords: bacterial pathogens; disease resistance; effector proteins; type three secretion system; plants

Figure 1.

Interaction between baterial pathogens and plants: Plants sense the presence of bacteria via detection of pathogen‐associated molecular patterns (PAMPs) such as flagellin, lipopolysaccharides (LPS), elongation factors Tu (EF‐Tu) and cold shock proteins (CSP). PAMPs are detected by trans‐membrane pattern recognition receptors (PRRs) (e.g. FLS2, EFR, etc.), which activate a basal defence system known as pathogen‐triggered immunity, PTI (black arrow). Some bacteria counteract by modifying their PAMPs and/or secreting virulence factors to suppress PTI (red lines and arrows). Resistant plants express R proteins that detect the presence of pathogen effector proteins inside the plant cell, and then activate multiple defences including the hypersensitive response (HR), a form of programmed cell death (grey arrows). Most successful pathogens secrete new effectors to suppress this effectors‐triggered immunity (ETI) by blocking the HR (blue line).

Figure 2.

Direct and indirect recognition of bacterial effectors: (a) The bacterial pathogen R. solanacearum injects the effector protein PopP2 into the plant cell. PopP2 is detected by the disease‐resistance protein RRS1 via direct binding, which activates downstream signalling events leading to disease resistance. (b) Pseudomonas syringae injects the effector protein AvrPphB into the plant cell. AvrPphB functions as a protease to catalyse cleavage of the host kinase PBS1. This modification is detected by the disease resistance protein RPS5, which then activates disease resistance.

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Further Reading

Abramovitch RB, Janjusevic R, Stebbins CE and Martin GB (2006) Type III effector AvrPtoB requires intrinsic E3 ubiquitin ligase activity to suppress plant cell death and immunity. Proceedings of the National Academy of Sciences of the USA 103: 2851–2856.

Alfano JR and Collmer A (1996) Bacterial pathogens in plants: life up against the wall. Plant Cell 8: 1683–1698.

Alfano JR and Collmer A (2004) Type III secretion system effector proteins: double agents in bacterial disease and plant defense. Annual Review of Phytopathology 42: 385–414.

Nomura K, Melotto M and He SY (2005) Suppression of host defense in compatible plant‐Pseudomonas syringae interactions. Current Opinion in Plant Biology 8: 361–368.

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How to Cite close
Ade, Jules, and Innes, Roger W(Sep 2007) Resistance to Bacterial Pathogens in Plants. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0020091]