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000888609 020__ $$a978-3-95806-560-4
000888609 037__ $$aFZJ-2020-05065
000888609 1001_ $$0P:(DE-Juel1)161522$$aKraxner, Kim$$b0$$eCorresponding author
000888609 245__ $$aNovel insights into the transcriptional regulation of cell division in Corynebacterium glutamicum$$f2014-01-01 - 2020-12-07
000888609 260__ $$aJülich$$bForschungszentrum Jülich GmbH Zentralbibliothek, Verlag$$c2021
000888609 300__ $$aV, 83
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000888609 3367_ $$0PUB:(DE-HGF)11$$2PUB:(DE-HGF)$$aDissertation / PhD Thesis$$bphd$$mphd$$s1631273206_14749
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000888609 4900_ $$aSchriften des Forschungszentrums Jülich Reihe Schlüsseltechnologien / Key Technologies$$v241
000888609 502__ $$aDissertation, Heinrich-Heine-Universität Düsseldorf, 2020$$bDissertation$$cHeinrich-Heine-Universität Düsseldorf$$d2020
000888609 500__ $$aBiotechnologie 1
000888609 520__ $$aIn 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
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000888609 9141_ $$y2020
000888609 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)161522$$aForschungszentrum Jülich$$b0$$kFZJ
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