Spermine inhibits PAMP-induced ROS and Ca2+ burst and reshapes the transcriptional landscape of PAMP-triggered immunity in Arabidopsis

Putrescine and spermine trigger opposite effects on PAMP-induced ROS production associated with different Ca(2+)signals, ultimately leading to differential regulation of PAMP-induced gene expression and disease resistance to avirulent bacteria. Polyamines are small polycationic amines whose levels increase during defense. Previous studies support the contribution of the polyamine spermine to defense responses. However, the potential contribution of spermine to pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) has not been completely established. Here, we compared the contribution of spermine and putrescine to early and late PTI responses in Arabidopsis. We found that putrescine and spermine have opposite effects on PAMP-elicited reactive oxygen species (ROS) production, with putrescine increasing and spermine lowering the flg22-stimulated ROS burst. Through genetic and pharmacological approaches, we found that the inhibitory effect of spermine on flg22-elicited ROS production is independent of polyamine oxidation, nitric oxide, and salicylic acid signaling but resembles chemical inhibition of RBOHD (RESPIRATORY BURST OXIDASE HOMOLOG D). Spermine can also suppress ROS elicited by FLS2-independent but RBOHD-dependent pathways, thus pointing to compromised RBOHD activity. Consistent with this, we found that spermine but not putrescine dampens flg22-stimulated cytosolic Ca2+ influx. Finally, we found that both polyamines differentially reshape transcriptional responses during PTI and disease resistance to Pseudomonas syringae. Overall, we provide evidence for the differential contributions of putrescine and spermine to PTI, with an impact on plant defense.