The Kunkel Lab uses a combination of molecular and genetic approaches to identify both pathogen and plant genes that govern disease development in the P. syringae/A. thaliana interaction. These studies have led to important insights regarding the virulence mechanisms of P. syringae and demonstrated that the pathogen uses a variety of strategies to manipulate the hormone biology its hosts to promote disease. For example, our earlier work on jasmonic acid (JA) signaling in A. thaliana and the P. syringae virulence factor coronatine, a molecular mimic of the plant hormone JA-Isoleucine (JA-Ile, Fig. 4), showed that coronatine promotes P. syringae pathogenesis by modulating JA signaling within the plant (Kloek et al, 2001; Brooks, 2004; Brooks, 2005; Laurie-Berry, 2006).
Specifically, we and others showed that, in addition to Type III secreted effectors, P. syringae uses coronatine to promote pathogenesis. Coronatine acts through at least three different mechanisms: 1) promoting entry of P. syringae into leaf tissue by re-opening of stomata (Melotto et al, 2006), 2) promoting growth in the apoplast by suppressing salicylic acid (SA)-mediated defenses (Brooks et al, 2005), and 3) promoting disease lesion development via an SA-independent mechanism (Kloek et al, 2001; Laurie-Berry et al, 2006) (Fig. 5).
More recently we and others discovered that PtoDC3000 also can manipulate host auxin biology to promote disease.
