Quorum sensing (QS) is a population density-dependent regulatory system in bacteria that couples gene expression to cell density through accumulation of diffusible signaling molecules. Pectobacteria are causal agents of soft rot disease in a range of economically important crops. They rely on QS to coordinate their main virulence factor, production of plant cell wall degrading enzymes (PCWDEs). Plants have evolved an array of antimicrobial compounds to anticipate and cope with pathogens, of which essential oils (EOs) are widely recognized. Here, volatile EOs, carvacrol and eugenol, were shown to specifically interfere with QS, the master regulator of virulence in pectobacteria, resulting in strong inhibition of QS genes, biofilm formation and PCWDEs, thereby leading to impaired infection. Accumulation of the signal molecule N-acylhomoserine lactone declined upon treatment with EOs, suggesting direct interaction of EOs with either homoserine lactone synthase (ExpI) or with the regulatory protein (ExpR). Homology models of both proteins were constructed and docking simulations were performed to test the above hypotheses. The resulting binding modes and docking scores of carvacrol and eugenol support potential binding to ExpI/ExpR, with stronger interactions than previously known inhibitors of both proteins. The results demonstrate the potential involvement of phytochemicals in the control of Pectobacterium.

Summary: The capability of Pectobacterium carotovorum isolates to infect monocotyledonous plants has been previously reported; however, no full consideration was given to characterize the association between such isolates and their monocot hosts. To assess differences in aggressiveness among P. carotovorum ssp. carotovorum isolates originating from monocotyledonous or dicotyledonous plants, we used as model plants two susceptible monocot hosts, the ornamentals Zantedeschia aethiopica and Ornithogalum dubium , as well as two common dicot hosts, Solanum tuberosum and Brassica oleracea . Using virulence assays and different genetic analyses we characterized P. carotovorum ssp. carotovorum isolates from diverse geographical locations which originated from plants belonging to four unrelated orders of monocots and five orders of dicots. Invariably, isolates originating from monocots exhibited higher virulence towards the tested monocot plants than dicot isolates, independently of their geographical source. Moreover, monocot and dicot isolates were clearly differentiated by various genetic analyses, such as 16S rRNA sequence clustering, intergenic transcribed spacer‐PCR (ITS‐PCR) banding pattern and amplified fragment length polymorphism (AFLP). We propose that the observed relationship between pathogenicity and genetic diversity among P. carotovorum ssp. carotovorum isolates reveals a co‐evolutionary specialization trend in the interaction between this pathogen and its hosts.

In the battle between bacteria and plants, bacteria often use a population density–dependent regulatory system known as quorum sensing (QS) to coordinate virulence gene expression. In response, plants use innate and induced defense mechanisms that include low-molecular-weight compounds, some of which serve as antivirulence agents by interfering with the QS machinery. The best-characterized QS system is driven by the autoinducer N-acyl-homoserine lactone (AHL), which is produced by AHL synthases (LuxI homologs) and perceived by response regulators (LuxR homologs). Several plant compounds have been shown to directly inhibit LuxI or LuxR. Gaining atomic-level insight into their mode of action and how they interfere with QS enzymes supports the identification and design of novel QS inhibitors.Such information can be gained by combining experimental work with molecular modeling and docking simulations. The summary of these findings shows that plant-derived compounds act as interkingdom cues and that these allomones specifically target bacterial communication systems.