Exit Seminar - Mechanisms by which beneficial Pseudomonas suppress plant immunity and protect them from pathogens

Sponsored by UBC Department of Microbiology & Immunology

Abstract: Plant roots associate with diverse microbial communities that include pathogenic microbes and commensals. Plants make use of their innate immune system to monitor microbiota by recognizing conserved microbe-associated molecular patterns (MAMPs). Despite containing identical MAMPs as pathogens, commensals persist in the rhizosphere indicating that they must suppress or evade host immunity. My work shows that beneficial Pseudomonas suppress host immunity via rhizosphere acidification through two distinct mechanisms. I found that rhizosphere acidification and gluconic acid biosynthesis is necessary for immunity suppression in an opportunistic pathogen Pseudomonas aeruginosaPAO1. However, I found a Pseudomonas simae WCS417 ∆pqqF mutant can still suppress flg22-induced immunity as indicated by activation of a transgenetic immunity reporter (CYP71A12_pro:GUS), indicating a distinct mechanism of host immunity suppression by WCS417. We performed a forward genetic screen in EMS mutagenized WCS417 to identify mutants that were unable to suppress the flg22-stimulated CYP71A12_pro:GUS expression. We found an ornithine carbamoyltransferase argF mutant lost the immunity suppression and rhizosphere acidification. Although argF is auxotrophic, I found that argF is required for host immunity suppression and rhizosphere acidification by preventing accumulation of ornithine, an alkaline precursor to arginine biosynthesis. Therefore, we uncovered two pathways, through organic acid biosynthesis, and conversion of alkaline ornithine to amino acids, work in synergy to acidify the rhizosphere and the resulting host immunity suppression.

In addition to modulation of host immunity, commensals are known to protect plants from pathogens. Pseudomonas sp. WCS365 robustly protects plants from a phylogenetically closely related opportunistic pathogen Pseudomonas sp. N2C3 in the rhizosphere. To uncover the mechanism of protection, I screened a collection of WCS365 biofilm formation transposon insertion mutants with surface attachment defects (sad) on an abiotic surface. I found that only a subset of sad mutants lost protection against the N2C3 pathogen implying distinct mechanisms of biofilm formation in vitro versus in planta. All the unprotective strains showed rhizosphere fitness defects suggesting that biofilm formation is necessary for bacterial colonization and protection.

Collectively, my work sheds light on our understanding of beneficial bacteria-mediated host immunity manipulation and protection of plants from pathogens.