In Pseudomonas syringae pv. phaseolicola NPS3121 the Regulator HrpL is Required for Siderophore Biosynthesis

The ability of P. syringae pv. phaseolicola to cause halo blight in bean cultivars is mainly determined by pathogenicity and virulence factors. An important pathogenicity component of P. syringae pv. phaseolicola is the type III secretion system (T3SS) that allows the secretion of effector proteins within the host cells, suppressing and modulating the host defense system. The hrpL gene encodes an alternative sigma factor, HrpL, essential for expressing genes involved in forming the T3SS. In several P. syringae pathovars, the biosynthesis of T3SS, siderophores, and some phytotoxins are coordinated by the GacS/GacA system. However, the regulatory connection between the GacS/GacA system, hrp intermediary regulators, and genes involved in synthesizing virulence factors is not fully described. In this study, the participation of HrpL in the production of phaseolotoxin and siderophores in P. syringae pv. phaseolicola NPS3121 was evaluated. An effective knockout strategy allowed the mutating of the hrpL gene. The mutation abolished the transcription of hrpL ; consequently, the mutant was unable to cause disease on bean pods. Phaseolotoxin and siderophore analysis revealed that in P. syringae pv. phaseolicola NPS3121, HrpL does not regulate the phaseolotoxin synthesis but is necessary to control siderophore biosynthesis. HrpL controls siderophore biosynthesis by the fur gene regulation. These results reveal a new transcriptional regulatory connection between HrpL and the control of siderophore biosynthesis. The study of these regulatory systems becomes significant in strengthening the understanding of bacterial pathogenesis.