RT Journal Article SR Electronic(1) A1 Sadykov, Marat R. A1 Hartmann, Torsten A1 Mattes, Theodoric A. A1 Hiatt, Megan A1 Jann, Naja J. A1 Zhu, Yefei A1 Ledala, Nagender A1 Landmann, Regine A1 Herrmann, Mathias A1 Rohde, Holger A1 Bischoff, Markus A1 Somerville, Greg A.YR 2011 T1 CcpA coordinates central metabolism and biofilm formation in Staphylococcus epidermidis JF Microbiology, VO 157 IS 12 SP 3458 OP 3468 DO https://doi.org/10.1099/mic.0.051243-0 PB Microbiology Society, SN 1465-2080, AB Staphylococcus epidermidis is an opportunistic bacterium whose infections often involve the formation of a biofilm on implanted biomaterials. In S. epidermidis, the exopolysaccharide facilitating bacterial adherence in a biofilm is polysaccharide intercellular adhesin (PIA), whose synthesis requires the enzymes encoded within the intercellular adhesin operon (icaADBC). In vitro, the formation of S. epidermidis biofilms is enhanced by conditions that repress tricarboxylic acid (TCA) cycle activity, such as growth in a medium containing glucose. In many Gram-positive bacteria, repression of TCA cycle genes in response to glucose is accomplished by catabolite control protein A (CcpA). CcpA is a member of the GalR–LacI repressor family that mediates carbon catabolite repression, leading us to hypothesize that catabolite control of S. epidermidis biofilm formation is indirectly regulated by CcpA-dependent repression of the TCA cycle. To test this hypothesis, ccpA deletion mutants were constructed in strain 1457 and 1457-acnA and the effects on TCA cycle activity, biofilm formation and virulence were assessed. As anticipated, deletion of ccpA derepressed TCA cycle activity and inhibited biofilm formation; however, ccpA deletion had only a modest effect on icaADBC transcription. Surprisingly, deletion of ccpA in strain 1457-acnA, a strain whose TCA cycle is inactive and where icaADBC transcription is derepressed, strongly inhibited icaADBC transcription. These observations demonstrate that CcpA is a positive effector of biofilm formation and icaADBC transcription and a repressor of TCA cycle activity., UL https://www.microbiologyresearch.org/content/journal/micro/10.1099/mic.0.051243-0