Pseudomonas bacteriocin syringacin M released upon desiccation suppresses the growth of sensitive bacteria in plant necrotic lesions.

Bacteriocins are regarded as important factors mediating microbial interactions, but their exact role in community ecology largely remains to be elucidated. Here, we report the characterization of a mutant strain, derived from Pseudomonas syringae pv. tomato DC3000 (Pst), that was incapable of growing in plant extracts and causing disease. Results showed that deficiency in a previously unannotated gene saxE led to the sensitivity of the mutant to Ca2+ in leaf extracts. Transposon insertions in the bacteriocin gene syrM, adjacent to saxE, fully rescued the bacterial virulence and growth of the ΔsaxE mutant in plant extracts, indicating that syrM-saxE encode a pair of bacteriocin immunity proteins in Pst. To investigate whether the syrM-saxE system conferred any advantage to Pst in competition with other SyrM-sensitive pathovars, we compared the growth of a SyrM-sensitive strain co-inoculated with Pst strains with or without the syrM gene and observed a significant syrM-dependent growth reduction of the sensitive bacteria on plate and in lesion tissues upon desiccation-rehydration treatment. These findings reveal an important biological role of SyrM-like bacteriocins and help to understand the complex strategies used by P. syringae in adaptation to the phyllosphere niche in the context of plant disease.