Skip to main content
. 2010 Jan 29;5(1):e8977. doi: 10.1371/journal.pone.0008977

Figure 7. Potential mechanisms underlying the effect of A. tumefaciens on P. syringae-plant interactions.

Figure 7

(A) A. tumefaciens inhibits proliferation or virulence gene expression in P. syringae. The presence of high densities of A. tumefaciens in the plant apoplast could have a direct inhibitory effect on proliferation and virulence gene expression in P. syringae. This, in turn, could enhance PAMP-triggered immunity (PTI) elicited by P. syringae MAMPS and suppress SA production. Infiltration of AtGV3101 also enhances some basal defence responses and ABA levels are reduced. (B) A. tumefaciens-mediated priming of the basal immune response inhibits proliferation or virulence gene expression in P. syringae. The observation that heat-killed AtGV3101 partially suppresses P. syringae-elicited SA argues against a direct interaction between AtGV3101 and P. syringae as the sole cause for SA suppression and enhanced expression of basal defences. An alternative explanation would be that AtGV3101 primes for an enhanced basal immune response, which has a negative effect on the ability of P. syringae to suppress PTI, and on the ability of P. syringae to elicit salicylic acid (SA) synthesis as a result of effector-triggered immunity (ETI) or disease. (C) A. tumefaciens-mediated priming of the basal immune response suppresses SA and ABA synthesis. In addition to inhibiting the activities of P. syringae, an enhanced basal immune response could directly suppress both SA and ABA synthesis. CW: cell wall; PM: plasma membrane; ABA: abscisic acid; MAMPs: microbe-associated molecular patterns.