The two-component system GrvRS (EtaRS) regulates ace expression in Enterococcus faecalis OG1RF.
Expression of ace (adhesin to collagen of Enterococcus faecalis), encoding a virulence factor in endocarditis and urinary tract infection models, has been shown to increase under certain conditions, such as in the presence of serum, bile salts, urine, and collagen and at 46 °C. However, the mechanism of ace/Ace regulation under different conditions is still unknown. In this study, we identified a two-component regulatory system GrvRS as the main regulator of ace expression under these stress conditions. Using Northern hybridization and β-galactosidase assays of an ace promoter-lacZ fusion, we found transcription of ace to be virtually absent in a grvR deletion mutant under the conditions that increase ace expression in wild-type OG1RF and in the complemented strain. Moreover, a grvR mutant revealed decreased collagen binding and biofilm formation as well as attenuation in a murine urinary tract infection model. Here we show that GrvR plays a major role in control of ace expression and E. faecalis virulence.
Division of Infectious Diseases, Department of Internal Medicine, The University of Texas Medical School, Houston, Texas, USA Center for the Study of Emerging and Re-emerging Pathogens, The University of Texas Medical School, Houston, Texas, USA Jung.H.Roh@uth.tmc.edu.
Jung Hyeob
JH
Roh
Division of Infectious Diseases, Department of Internal Medicine, The University of Texas Medical School, Houston, Texas, USA Center for the Study of Emerging and Re-emerging Pathogens, The University of Texas Medical School, Houston, Texas, USA.
Kavindra V
KV
Singh
Division of Infectious Diseases, Department of Internal Medicine, The University of Texas Medical School, Houston, Texas, USA Department of Chemistry, Biotechnology and Food Science, Laboratory of Microbial Gene Technology and Food Microbiology, Norwegian University of Life Sciences, Ås, Norway.
Sabina Leanti
SL
La Rosa
Division of Infectious Diseases, Department of Internal Medicine, The University of Texas Medical School, Houston, Texas, USA Center for Infectious and Inflammatory Diseases, Institute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, Texas, USA.
Ana Luisa V
AL
Cohen
Division of Infectious Diseases, Department of Internal Medicine, The University of Texas Medical School, Houston, Texas, USA Center for the Study of Emerging and Re-emerging Pathogens, The University of Texas Medical School, Houston, Texas, USA Department of Microbiology and Molecular Genetics, The University of Texas Medical School, Houston, Texas, USA.
Barbara E
BE
Murray
D000818:Animals; D019677:Artificial Gene Fusion; D001426:Bacterial Proteins / Q000096:biosynthesis* / Q000235:genetics; D015152:Blotting, Northern; D002352:Carrier Proteins / Q000096:biosynthesis* / Q000235:genetics; D004195:Disease Models, Animal; D013293:Enterococcus faecalis / Q000235:genetics* / Q000378:metabolism; D017353:Gene Deletion; D020869:Gene Expression Profiling; D015964:Gene Expression Regulation, Bacterial; D017930:Genes, Reporter; D005816:Genetic Complementation Test; D016908:Gram-Positive Bacterial Infections / Q000382:microbiology / Q000473:pathology; D051379:Mice; D014157:Transcription Factors / Q000378:metabolism*; D014552:Urinary Tract Infections / Q000382:microbiology / Q000473:pathology; D001616:beta-Galactosidase / Q000032:analysis / Q000235:genetics
C121675:Ace protein, Enterococcus; D001426:Bacterial Proteins; D002352:Carrier Proteins; D014157:Transcription Factors; D001616:beta-Galactosidase