Fig. 7.

Schematic presentation of entry and exit of A. tumefaciens infection. (A) Infection entry at the beginning of bacterial infection. The plant signal acetosyringone is released upon wounds to bind with sensor VirA and thereby activates VirG by phosphorylation. Activated VirG triggers vir gene expression and initiates T-DNA synthesis in A. tumefaciens. Bacterial type IV secretion system (T4SS) transfers T-DNA into plant cells and integrates into the plant chromosome. At this stage, salicylic acid (SA) is inactivated by conjugation with glucose to produce SAG in plant cells, SA-responsive genes are not induced, and genes encoding systematic acquired resistance (SAR) are turned off. In the bacterial cell, quorum quenching gene attM and SA hydrolase gene sghA are suppressed by AttJ and SghR, respectively. (B) Infection exit at the later stage of infection. Sucrose enhances at the wounded site during healing and is transported into bacterial cells to dissociate SghR from its complex with the promoter DNA inducing sghA expression. Accumulated SghA hydrolyzes SAG to release SA, which, on one hand, triggers the expression of the AttJ-AttKLM operon, thus initiating quorum quenching and γ-aminobutyric acid (GABA) catabolism systems inside the bacterial cells. On the other hand, released SA inactivates VirA to shut down infection machinery. Additionally, released SA could also activate plant SA responsive genes and SAR.