Control of pili synthesis and putrescine homeostasis inEscherichia coli

Abstract

SummaryPolyamines are biologically ubiquitous cations that bind to nucleic acids, ribosomes, and phospholipids and, thereby, modulate numerous processes, including surface motility inEscherichia coli. We characterized the metabolic and transcription factors that contribute to polyamine-dependent control of surface motility. Genetic analysis showed that surface motility required type 1 pili and the simultaneous presence of two independent putrescine anabolic pathways and that putrescine transport and catabolism modulated surface motility. The results of an immunological assay for FimA—the major pili subunit, reverse transcription quantitative PCR offimA, and transmission electron microscopy confirmed that pili synthesis required putrescine. RNAseq analysis of a parental and putrescine-deficient mutant and a follow-up genetic analysis suggested that H-NS was the putrescine-responsive regulator of pili synthesis and surface motility. The RNAseq results also showed that low putrescine increased transcripts for genes of arginine synthesis and transport systems for magnesium and phosphate, and decreased transcripts of genes for oxidative energy metabolism and iron transport. We conclude that (a) putrescine controls pili synthesis and surface motility possibly via the transcriptional regulator H-NS, and (b) a complex homeostatic network, which can rewire metabolism, controls putrescine concentrations. During a urinary tract infection, the polyamine putrescine is present in urine and pili are required for the binding of bacteria to the bladder epithelium. Because of its control of pili synthesis and energy metabolism, putrescine is likely to contribute to the establishment and maintenance of urinary tract infections associated with uropathogenicEscherichia coli.