IS256 abolishes gelatinase activity and biofilm formation in a mutant of the nosocomial pathogen Enterococcus faecalis V583

Abstract

Enterococcus faecalis is one of the most controversial species of lactic acid bacteria. Some strains are used as probiotics, while others are associated with severe and life-threatening nosocomial infections. Their pathogenicity depends on the acquisition of multidrug resistance and virulence factors. Gelatinase, which is required in the first steps of biofilm formation, is an important virulence determinant involved in E. faecalis pathogenesis, including endocarditis and peritonitis. The gene that codes for gelatinase (gelE) is controlled by the Fsr quorum-sensing system, whose encoding genes (fsrA, fsrB, fsrC, and fsrD) are located immediately upstream of gelE. The integration of a DNA fragment into the fsr locus of a derived mutant of E. faecalis V583 suppressed the gelatinase activity and prevented biofilm formation. Sequence analysis indicated the presence of IS256 integrated into the fsrC gene at nucleotide position 321. Interestingly, IS256 is also associated with biofilm formation in Staphylococcus epidermidis and Staphylococcus aureus. This is the first description of an insertion sequence that prevents biofilm formation in E. faecalis.

High abundance and expression of transposases in bacteria from the Baltic Sea

“…This cluster contains genes necessary for generating both green and red pigmentation and in some cases also two transposases, suggesting a role of transposases in the HGT event that formed the cluster ( Larsson et al , 2014 ). In Staphylococcus and Pseudoalteromonas , the switch between planktonic and biofilm forming phenotypes (phase variation) is regulated via reversible insertion/excision of IS256 family transposases into biofilm-essential genes ( Ziebuhr et al , 1999 ; Valle et al , 2007 ; Hennig and Ziebuhr, 2008 ; Perez et al , 2015 ). Such transposition events are in turn regulated by the global stress response regulator σ B ( Valle et al , 2007 ).…”

The impact of insertion sequences on bacterial genome plasticity and adaptability

“…IS256 has also been found to indirectly affect ica expression by inactivating rsbU (a positive regulator of the global stress response sigma factor r B ) or sarA (encoding the staphylococcal accessory regulator) (Conlon et al 2004). In Enterococcus faecalis, IS256 transposition mediated inactivation of gelatinase activity, which is essential in the initial steps of biofilm formation (Perez et al 2015). Loss of extracellular polysaccharide production was also observed in Xanthomonas oryzaei via IS-mediated inactivation of the gumM gene, which is part of the gum cluster involved in the biosynthesis of extracellular polysaccharides (Rajeshwari & Sonti 2000).…”

Biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin

“…Associations between some of these genes and biofilm formation have been recognized (e.g., gelE 11, 19 ); yet, no study has systematically investigated whether the complete or partial presence of this gene set is a predictor of the biofilm formation phenotype. Such correlation would be of great diagnostic value, but is hindered by poor metadata available about published enterococcal genomes, which impede attempts for comparative genomics between biofilm and non-biofilm formers.…”