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dc.contributor.authorEckelt, Elke
dc.contributor.authorMeißner, Thorsten
dc.contributor.authorMeens, Jochen
dc.contributor.authorLaarmann, Kristin
dc.contributor.authorNerlich, Andreas
dc.contributor.authorJarek, Michael
dc.contributor.authorWeiss, Siegfried
dc.contributor.authorGerlach, Gerald-F
dc.contributor.authorGoethe, Ralph
dc.date.accessioned2015-10-29T11:45:45Zen
dc.date.available2015-10-29T11:45:45Zen
dc.date.issued2015en
dc.identifier.citationFurA contributes to the oxidative stress response regulation of Mycobacterium avium ssp. paratuberculosis. 2015, 6:16 Front Microbiolen
dc.identifier.issn1664-302Xen
dc.identifier.pmid25705205en
dc.identifier.doi10.3389/fmicb.2015.00016en
dc.identifier.urihttp://hdl.handle.net/10033/581416en
dc.description.abstractThe ferric uptake regulator A (FurA) is known to be involved in iron homeostasis and stress response in many bacteria. In mycobacteria the precise role of FurA is still unclear. In the presented study, we addressed the functional role of FurA in the ruminant pathogen Mycobacterium avium ssp. paratuberculosis (MAP) by construction of a furA deletion strain (MAPΔfurA). RNA deep sequencing revealed that the FurA regulon consists of repressed and activated genes associated to stress response or intracellular survival. Not a single gene related to metal homeostasis was affected by furA deletion. A decisive role of FurA during intracellular survival in macrophages was shown by significantly enhanced survival of MAPΔfurA compared to the wildtype, indicating that a principal task of mycobacterial FurA is oxidative stress response regulation in macrophages. This resistance was not associated with altered survival of mice after long term infection with MAP. Our results demonstrate for the first time, that mycobacterial FurA is not involved in the regulation of iron homeostasis. However, they provide strong evidence that FurA contributes to intracellular survival as an oxidative stress sensing regulator.
dc.language.isoenen
dc.titleFurA contributes to the oxidative stress response regulation of Mycobacterium avium ssp. paratuberculosis.en
dc.typeArticleen
dc.contributor.departmentHZI-Helmholzzentrum für Infektionsforschungen
dc.identifier.journalFrontiers in microbiologyen
refterms.dateFOA2018-06-12T16:41:12Z
html.description.abstractThe ferric uptake regulator A (FurA) is known to be involved in iron homeostasis and stress response in many bacteria. In mycobacteria the precise role of FurA is still unclear. In the presented study, we addressed the functional role of FurA in the ruminant pathogen Mycobacterium avium ssp. paratuberculosis (MAP) by construction of a furA deletion strain (MAPΔfurA). RNA deep sequencing revealed that the FurA regulon consists of repressed and activated genes associated to stress response or intracellular survival. Not a single gene related to metal homeostasis was affected by furA deletion. A decisive role of FurA during intracellular survival in macrophages was shown by significantly enhanced survival of MAPΔfurA compared to the wildtype, indicating that a principal task of mycobacterial FurA is oxidative stress response regulation in macrophages. This resistance was not associated with altered survival of mice after long term infection with MAP. Our results demonstrate for the first time, that mycobacterial FurA is not involved in the regulation of iron homeostasis. However, they provide strong evidence that FurA contributes to intracellular survival as an oxidative stress sensing regulator.


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