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Rhodopseudomonas palustris quorum sensing molecule pC-HSL induces systemic resistance to TMV infection via up-regulation of NbSIPK/NbWIPK expressions in Nicotiana benthamiana.

G-negative bacteria produce a myriad of N-acyl-homoserine lactones (AHLs) that can function as quorum sensing (QS) signaling molecules. AHLs are also known to regulate various plant biological activities. p-Coumaroyl-homoserine lactone (pC-HSL) is the only QS molecule produced by a photosynthetic bacterium, Rhodopseudomonas palustris (R. palustris). The role of pC-HSL in the interaction between R. palustris and plant has not been investigated. In this study, we investigated the effect of pC-HSL on plant immunity and have found that this QS molecule can induce a systemic resistance to Tobacco mosaic virus (TMV) infection in Nicotiana benthamiana (N. benthamiana). The results show that pC-HSL treatment can prolong the activation of two mitogen-associated protein kinase (MAPK) genes (i.e., NbSIPK and NbWIPK) and enhance the expression of transcription factor WRKY8 as well as immune response marker genes NbPR1 and NbPR10, leading to an increased accumulation of reactive oxygen species (ROS) in the TMV infected plants. Our results also show that pC-HSL treatment can increase activities of two ROS-scavenging enzymes, POD and SOD. Knockdown of NbSIPK or NbWIPK expression in N. benthamiana plants through VIGS nullified or attenuated pC-HSL-induced systemic resistance, indicating that the functioning of pC-HSL relies on the activity of those two kinases. Meanwhile, pC-HSL pre-treated plants also showed a strong induction of kinase activities of NbSIPK and NbWIPK post TMV inoculation. Taken together, our results demonstrate that pC-HSL treatment results in enhanced plant resistance to TMV infection, which is helpful to uncover the outcome of interaction between R. palustris and its host plants.