Role of cell division protein divIVA in Enterococcus faecalis pathogenesis, biofilm and drug resistance: A future perspective by in silico approaches.

Antibiotics resistance is the major problem in clinical settings which leads to the emergence of drug resistant bacteria. Biofilm formation is one of the grounds for the emergence of antibiotics resistant strains of Enterococcus faecalis. Our group previously reported in a comparative proteomic study of biofilm and planktonic state of E. faecalis that cell division protein divIVA was two folds overexpressed in biofilm state as compared to planktonic one and suggested its involvement in biofilm formation and antibiotics resistance. In this in silico study molecular docking showed that DNA bind to the conserved amino acid residues of divIVA domain and suggested that divIVA possibly secretes DNA into extra polymeric substance (EPS) which is the part of biofilm. We also performed the STRING analysis of cell division protein divIVA and predicted their interactive partners {cell division proteins/divisome complex (ftsZ, ftsA, divIV, ftsL, & gpsB), hypothetical proteins (sepF, EF_0261, EF_1000, EF_0998, EF_1006 & EF_1040), isoleucyl-tRNA synthetase (ileS), septation ring formation regulator (ezrA), S4 domain-containing protein (EF_1001), rod shape-determining protein (mreC), UDP-N-acetylmuramoyl-L-alanyl-d-glutamate synthetase (murD), UDP-diphospho-muramoyl-pentapeptide beta-N- acetylglucosaminyltransferase (murG), Lipoprotein signal peptidase (lspA), adenylate kinase (adk) and DNA-binding response regulator (vicR)}. We suggest that cumulatively divIVA and its interactive partners might be directly or indirectly involved in E. faecalis cell division, growth, biofilm formation, virulence and resistance.