| The bacterial plant pathogen Pseudomonas syringae secretes various virulence factors during infection. One such factor, AvrRpt2, is secreted directly into the plant cell through the type III secretion system. In my thesis, I first demonstrated that AvrRpt2 functions from inside plant cells to promote P. syringae virulence on Arabidopsis thaliana . I next investigated mechanism(s) underlying the virulence activity of AvrRpt2, and observed that AvrRpt2 suppresses the expression of several plant defense genes, suggesting that AvrRpt2 functions by suppressing host defenses. However, since AvrRpt2 promotes the growth of P. syringae on A. thaliana plants that are unable to accumulate the plant defense hormone salicylic acid (SA), AvrRpt2 appears to function downstream or independently of SA. Additionally, I observed that expression of AvrRpt2 in transgenic A. thaliana plants causes seedling phenotypes reminiscent of plants with altered auxin physiology. AvrRpt2 transgenic seedlings also exhibit increased sensitivity to the auxin analog 2,4-D, and accumulate higher levels of free indole-3-acetic acid (IAA), the predominant naturally occurring auxin. These results, in conjunction with the observation that the presence of AvrRpt2 is associated with an increase in free IAA levels in P. syringae-infected mature plants, indicate that AvrRpt2 alters host auxin physiology. I further investigated whether alterations in host auxin physiology affect P. syringae pathogenesis, and obtained evidence suggesting that an increase in free IAA levels promotes P. syringae virulence, and that intact auxin signaling is required for full disease susceptibility in A. thaliana . Thus, the discovery that AvrRpt2 alters host auxin physiology suggests an additional (or alternative) mechanism by which AvrRpt2 promotes P. syringae virulence.; While studying the involvement of auxin physiology in P. syringae pathogenesis, I observed that infection by P. syringae resulted both in the up-regulation of A. thaliana genes encoding enzymes involved in production of free IAA, and in an increase in free IAA levels. I also observed that the full induction of two of these genes was dependent on the ability of P. syringae to synthesize the phytotoxin coronatine, an important virulence factor. These results suggest that P. syringae actively modulates the production of free IAA during infection to promote virulence. |
