Marat Sadykov

Publications (2)8.07 Total impact

• Article: CcpA coordinates central metabolism and biofilm formation in Staphylococcus epidermidis.

  Marat R Sadykov, Torsten Hartmann, Theodoric A Mattes, Megan Hiatt, Naja J Jann, Yefei Zhu, Nagender Ledala, Regine Landmann, Mathias Herrmann, Holger Rohde, Markus Bischoff, Greg A Somerville
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  ABSTRACT: 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.
  Microbiology 09/2011; 157(Pt 12):3458-68. · 3.06 Impact Factor
• Article: Multiplication of a restriction-modification gene complex.

  Marat Sadykov, Yasuo Asami, Hironori Niki, Naofumi Handa, Mitsuhiro Itaya, Masaru Tanokura, Ichizo Kobayashi
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  ABSTRACT: Previous works have suggested that some gene complexes encoding a restriction (R) enzyme and a cognate modification (M) enzyme may behave as selfish mobile genetic elements. RM gene complexes, which destroy 'non-self' elements marked by the absence of proper methylation, are often associated with mobile genetic elements and are involved in various genome rearrangements. Here, we found amplification of a restriction-modification gene complex. BamHI gene complex inserted into the Bacillus chromosome showed resistance to replacement by a homologous stretch of DNA. Some cells became transformed with the donor without losing BamHI. In most of these transformants, multiple copies of BamHI and the donor allele were arranged as tandem repeats. When a clone carrying one copy of each allele was propagated, extensive amplification of BamHI and the donor unit was observed in a manner dependent on restriction enzyme gene. This suggests that restriction cutting of the genome participates in the amplification. Visualization by fluorescent in situ hybridization revealed that the amplification occurred in single cells in a burst-like fashion that is reminiscent of induction of provirus replication. The multiplication ability in a bacterium with natural capacity for DNA release, uptake and transformation will be discussed in relation to spreading of RM gene -complexes.
  Molecular Microbiology 05/2003; 48(2):417-27. · 5.01 Impact Factor