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@PHDTHESIS{Kraxner:888609,
      author       = {Kraxner, Kim},
      title        = {{N}ovel insights into the transcriptional regulation of
                      cell division in {C}orynebacterium glutamicum},
      volume       = {241},
      school       = {Heinrich-Heine-Universität Düsseldorf},
      type         = {Dissertation},
      address      = {Jülich},
      publisher    = {Forschungszentrum Jülich GmbH Zentralbibliothek, Verlag},
      reportid     = {FZJ-2020-05065},
      isbn         = {978-3-95806-560-4},
      series       = {Schriften des Forschungszentrums Jülich Reihe
                      Schlüsseltechnologien / Key Technologies},
      pages        = {V, 83},
      year         = {2021},
      note         = {Biotechnologie 1; Dissertation, Heinrich-Heine-Universität
                      Düsseldorf, 2020},
      abstract     = {In the first part of this doctoral thesis the
                      transcriptional regulation of the odhI gene (cg1630)of
                      Corynebacterium glutamicum was analyzed. OdhI in its
                      unphoshorylated state functions asinhibitor of the
                      2-oxoglutarate dehydrogenase complex (ODHC) by binding to
                      the OdhAsubunit. Phosphorylation of OdhI by serine/threonine
                      protein kinases abolishes this effect.Inhibition of ODHC
                      activity by OdhI was shown to be crucial for overproduction
                      and secretionof L-glutamate, which is used as a flavour
                      enhancer. Since downstream of odhI two genespresumably
                      encoding transcriptional regulators (cg1631 and cg1633) are
                      located, it wasspeculated that these could be involved in
                      transcriptional regulation of odhI. However,transcriptome
                      analysis of deletion mutants lacking cg1631 or cg1633 and
                      DNA affinitychromatography with the odhI promoter did not
                      support this hypothesis. Furthermore, no otherpotential
                      transcriptional regulators of odhI could be identified.
                      Thus, there is currently noevidence for transcriptional
                      regulation of odhI.The second part of this thesis addresses
                      the regulation of cytokinesis in C. glutamicum. Incontrast
                      to e.g. Escherichia coli and Bacillus subtilis, knowledge
                      about regulators of cytokinesisin Actinobacteria is very
                      limited. In this study, the so far uncharacterized Cg1631
                      protein wasdiscovered to be a transcriptional regulator of
                      the ftsZ gene in C. glutamicum encoding the keyplayer of
                      bacterial cell division. Therefore, Cg1631 was named FtsR,
                      standing for FtsZregulator. Both deletion and overexpression
                      of ftsR caused growth defects and an altered cellmorphology,
                      emphasizing an important function of FtsR in cell division
                      or cell wall synthesis.The wild-type phenotype could be
                      restored by plasmid-based complementation. Chromatinaffinity
                      purification with subsequent next generation sequencing
                      (ChAP-Seq) identified a regionin the ftsZ promoter as a
                      major FtsR binding site, but revealed also additional
                      potential targetgenes. With the ChAP-Seq results a putative
                      DNA-binding motif could be identified for
                      FtsR.Transcriptional activation of ftsZ expression by FtsR
                      was underlined by DNA microarrayexperiments, electrophoretic
                      mobility shift assays (EMSAs), and reporter gene
                      studies.Analysis of strains expressing ftsZ under control of
                      the gluconate-inducible gntK promoterrevealed that the
                      phenotype of the ftsR mutant is not solely caused by
                      reduced ftsZexpression but involves additional factors. In
                      summary, FtsR was identified as the firsttranscriptional
                      regulator of ftsZ in C. glutamicum. Furthermore, since FtsR
                      and its DNA-bindingsite in the promoter region of ftsZ are
                      highly conserved in Actinobacteria, it can be assumedthat
                      this regulatory mechanism is also relevant for the control
                      of cell division in relatedActinobacteria. This makes FtsR a
                      promising target for the development of new
                      antimicrobialdrugs against pathogenic relatives of C.
                      glutamicum},
      cin          = {IBG-1},
      cid          = {I:(DE-Juel1)IBG-1-20101118},
      pnm          = {581 - Biotechnology (POF3-581)},
      pid          = {G:(DE-HGF)POF3-581},
      typ          = {PUB:(DE-HGF)3 / PUB:(DE-HGF)11},
      urn          = {urn:nbn:de:0001-2021100106},
      url          = {https://juser.fz-juelich.de/record/888609},
}