Polyamine-mediated mechanisms contribute to oxidative stress tolerance in Pseudomonas syringae.

Bacterial phytopathogens thriving in the surface or the interior of plants may experience oxidative stress because of the activation of plant defense responses. Polyamines have been proposed to participate in the protection of bacteria against this stress, but the mechanisms behind their functions are mostly unclear. In this study, we sought to understand the effects of oxidative stress on the polyamine homeostasis of the plant pathogen Pseudomonas syringae and decipher the functions of these compounds in stress tolerance. We showed that bacteria react to H 2 O 2 by raising the extracellular amount of the polyamine putrescine while the intracellular levels of this compound as well as the analogue spermidine remained unchanged. Consistent with this, supplementation of media with exogenous putrescine enhanced bacterial tolerance to H 2 O 2 . Deletion of arginine decarboxylase ( speA ) and ornithine decarboxylate ( speC ), prevented the synthesis of putrescine and augmented susceptibility to H 2 O 2 , whereas targeting spermidine synthesis alone through deletion of spermidine synthase ( speE ) increased the level of extracellular putrescine and enhanced H 2 O 2 tolerance. Further research demonstrated that the increased tolerance of the ΔspeE mutant correlated both with increased expression of H 2 O 2 -degrading catalases and enhanced outer cell membrane stability. Thus, this work demonstrates previously unidentified links between the metabolism of polyamines and the defense against oxidative stress in bacteria.