CcpA coordinates central metabolism and biofilm formation in Staphylococcus epidermidis.
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CcpA coordinates central metabolism and biofilm formation in Staphylococcus epidermidis. / Sadykov, Marat R; Hartmann, Torsten; Mattes, Theodoric A; Hiatt, Megan; Jann, Naja J; Zhu, Yefei; Ledala, Nagender; Landmann, Regine; Herrmann, Mathias; Rohde, Holger; Bischoff, Markus; Somerville, Greg A.
in: MICROBIOLOGY+, Jahrgang 157, Nr. Pt 12, Pt 12, 2011, S. 3458-3468.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - CcpA coordinates central metabolism and biofilm formation in Staphylococcus epidermidis.
AU - Sadykov, Marat R
AU - Hartmann, Torsten
AU - Mattes, Theodoric A
AU - Hiatt, Megan
AU - Jann, Naja J
AU - Zhu, Yefei
AU - Ledala, Nagender
AU - Landmann, Regine
AU - Herrmann, Mathias
AU - Rohde, Holger
AU - Bischoff, Markus
AU - Somerville, Greg A
PY - 2011
Y1 - 2011
N2 - 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.
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.
KW - Animals
KW - Humans
KW - Female
KW - Mice
KW - Gene Deletion
KW - Bacterial Proteins/genetics/metabolism
KW - Gene Expression Regulation, Bacterial
KW - Biofilms/growth & development
KW - Virulence
KW - Energy Metabolism
KW - Citric Acid Cycle/genetics
KW - Polysaccharides, Bacterial/metabolism
KW - Repressor Proteins/genetics/metabolism
KW - Staphylococcus epidermidis/genetics/growth & development/metabolism/physiology
KW - Animals
KW - Humans
KW - Female
KW - Mice
KW - Gene Deletion
KW - Bacterial Proteins/genetics/metabolism
KW - Gene Expression Regulation, Bacterial
KW - Biofilms/growth & development
KW - Virulence
KW - Energy Metabolism
KW - Citric Acid Cycle/genetics
KW - Polysaccharides, Bacterial/metabolism
KW - Repressor Proteins/genetics/metabolism
KW - Staphylococcus epidermidis/genetics/growth & development/metabolism/physiology
M3 - SCORING: Journal article
VL - 157
SP - 3458
EP - 3468
JO - MICROBIOLOGY+
JF - MICROBIOLOGY+
SN - 0026-2617
IS - Pt 12
M1 - Pt 12
ER -
