Fig. 6.

Indole-3-acetic acid (IAA) plays multiple roles during PtoDC3000 pathogenesis. A working model illustrates how IAA promotes PtoDC3000 pathogenesis via multiple mechanisms. Upon PtoDC3000 infection, detection of microbe associated molecular patterns (MAMPs) induces expression of basal host defense responses mediated by salicylic acid (SA). Early during infection expression of the T3S system (T3SS) allows delivery of effector proteins (blue shapes) into the host cell to suppress MAMP-induced defenses. PtoDC3000 infection results in elevated auxin (e.g., IAA) levels in infected tissue, possibly due to auxin synthesis by both the host and PtoDC3000 (via activity of the Indoleacetaldehyde dehydrogenase AldA (McClerklin et al. 2018). Disruption of host auxin signaling, for example by the dominant axr2–1 mutation, prevents suppression of SA defenses and results in reduced disease susceptibility. IAA also promotes the growth of PtoDC3000 independently of suppression of SA-mediated defenses, by regulating expression of pathogen virulence genes (green and purple block arrows). We hypothesize that IAA downregulates T3SS genes after they are no longer needed (e.g., 24 h postinfection), and activates virulence genes, such as tvrR, that are required at intermediate or late stages of infection. Genes that are transcribed are indicated by the small black arrowhead above the block arrows.