AbaM Regulates Quorum Sensing, Biofilm Formation, and Virulence in .

possesses a single divergent /-type quorum-sensing (QS) locus named / This locus also contains a third gene located between and , which we term , that codes for an uncharacterized member of the RsaM protein family known to regulate -acylhomoserine lactone (AHL)-dependent QS in other beta- and gammaproteobacteria. Here, we show that disruption of via a T26 insertion in strain AB5075 resulted in increased production of -(3-hydroxydodecanoyl)-l-homoserine lactone and enhanced surface motility and biofilm formation. In contrast to the wild type and the ::T26 mutant, the virulence of the ::T26 mutant was completely attenuated in a infection model. Transcriptomic analysis of the ::T26 mutant revealed that AbaM differentially regulates at least 76 genes, including the pilus operon and the acinetin 505 lipopeptide biosynthetic operon, that are involved in surface adherence, biofilm formation and virulence. A comparison of the wild type, ::T26 and ::T26 transcriptomes, indicates that AbaM regulates ∼21% of the QS regulon including the operon. Moreover, the QS genes ( and ) were among the most upregulated in the ::T26 mutant. -based reporter gene fusions revealed that expression is positively regulated by QS but negatively autoregulated. Overall, the data presented in this work demonstrates that AbaM plays a central role in regulating QS, virulence, surface motility, and biofilm formation. is a multiantibiotic-resistant pathogen of global health care importance. Understanding virulence gene regulation could aid the development of novel anti-infective strategies. In , the and genes that code for the receptor and synthase components of an -acylhomoserine (AHL) lactone-dependent quorum sensing system (QS) are separated by Here, we show that although mutation of increased AHL production, surface motility, and biofilm development, it resulted in the attenuation of virulence. AbaM was found to control both QS-dependent and QS-independent genes. The significance of this work lies in the identification of AbaM, an RsaM ortholog known to control virulence in plant pathogens, as a modulator of virulence in a human pathogen.