The iron-induced ferredoxin FdxA of Campylobacter jejuni is involved in aerotolerance

Vliet, Arnoud H. M. van

doi:10.1016/s0378-1097(01)00067-2

Cited by 39 publications

(39 citation statements)

References 15 publications

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“…From cluster B, the ferredoxin FdxA (with 14-fold induction at mid-log phase), is worth noting because these results confirm the previously reported induction of fdxA expression by iron (53). An fdxA mutant has been shown to be affected in its aerotolerance ability, suggesting a role for FdxA in oxidative stress defense (53). Clusters C and D contain genes that are antagonistically expressed between the two sets of experiments (the time course and the mid-log experiment).…”

Section: Resultssupporting

confidence: 86%

“…Of interest, the oxidoreductase OorABCD may have a function complementary to that of several of the putative iron-independent oxidoreductase enzymes listed in Table 4 (Cj0414, Cj0559, and Cj1287c) under iron-rich growth conditions. From cluster B, the ferredoxin FdxA (with 14-fold induction at mid-log phase), is worth noting because these results confirm the previously reported induction of fdxA expression by iron (53). An fdxA mutant has been shown to be affected in its aerotolerance ability, suggesting a role for FdxA in oxidative stress defense (53).…”

Section: Resultssupporting

confidence: 82%

“…As discussed above, FdxA is probably involved in oxidative stress defense. This protein has been proposed to reduce the oxidized state of the alkyl hydroxyperoxide reductase (AhpC), similar to AhpF in other gram-negative bacterium (53,54).…”

Section: Fig 2 Operon Mapping By Rt-pcr Analysis Of Iron-andmentioning

confidence: 99%

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Iron Acquisition and Regulation in Campylobacter jejuni

2004

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Iron affects the physiology of bacteria in two different ways: as a micronutrient for bacterial growth and as a catalyst for the formation of hydroxyl radicals. In this study, we used DNA microarrays to identify the C. jejuni genes that have their transcript abundance affected by iron availability. The transcript levels of 647 genes were affected after the addition of iron to iron-limited C. jejuni cells. Several classes of affected genes were revealed within 15 min, including immediate-early response genes as well as those specific to iron acquisition and metabolism. In contrast, only 208 genes were differentially expressed during steady-state experiments comparing iron-rich and iron-limited growth conditions. As expected, genes annotated as being involved in either iron acquisition or oxidative stress defense were downregulated during both time course and steady-state experiments, while genes encoding proteins involved in energy metabolism were upregulated. Because the level of protein glycosylation increased with iron limitation, iron may modulate the level of C. jejuni virulence by affecting the degree of protein glycosylation. Since iron homeostasis has been shown to be Fur regulated in C. jejuni, an isogenic fur mutant was used to define the Fur regulon by transcriptome profiling. A total of 53 genes were Fur regulated, including many genes not previously associated with Fur regulation. A putative Fur binding consensus sequence was identified in the promoter region of most iron-repressed and Fur-regulated genes. Interestingly, a fur mutant was found to be significantly affected in its ability to colonize the gastrointestinal tract of chicks, highlighting the importance of iron homeostasis in vivo. Directed mutagenesis of other genes identified by the microarray analyses allowed the characterization of the ferric enterobactin receptor, previously named CfrA. Chick colonization assays indicated that mutants defective in enterobactin-mediated iron acquisition were unable to colonize the gastrointestinal tract. In addition, a mutation in a receptor (Cj0178) for an uncharacterized iron source also resulted in reduced colonization potential. Overall, this work documents the complex response of C. jejuni to iron availability, describes the genetic network between the Fur and iron regulons, and provides insight regarding the role of iron in C. jejuni colonization in vivo.

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Section: Resultssupporting

confidence: 86%

Section: Resultssupporting

confidence: 82%

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Iron Acquisition and Regulation in Campylobacter jejuni

2004

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“…The mutants were confirmed by PCR and sequencing. To complement or supplement the cj1501 gene in C. jejuni strains, the gene was inserted together with a chloramphenicol resistance gene into the pseudogene cj0046 under the control of a native C. jejuni promoter, fdxA (36,39). This construct was then introduced into the C. jejuni wild-type strain and its isogenic cj1501 mutant by electroporation, followed by selection for chloramphenicol resistance.…”

Section: Methodsmentioning

confidence: 99%

Selenium-Dependent Biogenesis of Formate Dehydrogenase in Campylobacter jejuni Is Controlled by the fdhTU Accessory Genes

et al. 2012

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The food-borne bacterial pathogen Campylobacter jejuni efficiently utilizes organic acids such as lactate and formate for energy production. Formate is rapidly metabolized via the activity of the multisubunit formate dehydrogenase (FDH) enzyme, of which the FdhA subunit is predicted to contain a selenocysteine (SeC) amino acid. In this study we investigated the function of the cj1500 and cj1501 genes of C. jejuni, demonstrate that they are involved in selenium-controlled production of FDH, and propose the names fdhT and fdhU, respectively. Insertional inactivation of fdhT or fdhU in C. jejuni resulted in the absence of FdhA and FdhB protein expression, reduced fdhABC RNA levels, the absence of FDH enzyme activity, and the lack of formate utilization, as assessed by 1 H nuclear magnetic resonance. The fdhABC genes are transcribed from a single promoter located two genes upstream of fdhA, and the decrease in fdhABC RNA levels in the fdhU mutant is mediated at the posttranscriptional level. FDH activity and the ability to utilize formate were restored by genetic complementation with fdhU and by supplementation of the growth media with selenium dioxide. Disruption of SeC synthesis by inactivation of the selA and selB genes also resulted in the absence of FDH activity, which could not be restored by selenium supplementation. Comparative genomic analysis suggests a link between the presence of selA and fdhTU orthologs and the predicted presence of SeC in FdhA. The fdhTU genes encode accessory proteins required for FDH expression and activity in C. jejuni, possibly by contributing to acquisition or utilization of selenium.

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“…The heat shock protease HtrA and the regulator HspR have been shown to be important for short-term aerobic tolerance (3,12). The fdxA gene upstream of ahpC encodes a ferrodoxin that has been identified as important for aerotolerance (74). Also, SpoT, which regulates the C. jejuni stringent response, was found to be important for low CO 2 growth and aerobic survival (28).…”

mentioning

confidence: 99%

The Campylobacter jejuni Transcriptional Regulator Cj1556 Plays a Role in the Oxidative and Aerobic Stress Response and Is Important for Bacterial SurvivalIn Vivo

et al. 2011

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Campylobacter jejuni is the leading bacterial cause of human gastroenteritis worldwide. Despite stringent microaerobic growth requirements, C. jejuni is ubiquitous in the aerobic environment and so must possess regulatory systems to sense and adapt to external stimuli, such as oxidative and aerobic (O 2 ) stress. Reannotation of the C. jejuni NCTC11168 genome sequence identified Cj1556 (originally annotated as a hypothetical protein) as a MarR family transcriptional regulator, and further analysis indicated a potential role in regulating the oxidative stress response. A C. jejuni 11168H Cj1556 mutant exhibited increased sensitivity to oxidative and aerobic stress, decreased ability for intracellular survival in Caco-2 human intestinal epithelial cells and J774A.1 mouse macrophages, and a reduction in virulence in the Galleria mellonella infection model. Microarray analysis of gene expression changes in the Cj1556 mutant indicated negative autoregulation of Cj1556 expression and downregulation of genes associated with oxidative and aerobic stress responses, such as katA , perR , and hspR . Electrophoretic mobility shift assays confirmed the binding of recombinant Cj1556 to the promoter region upstream of the Cj1556 gene. cprS , which encodes a sensor kinase involved in regulation of biofilm formation, was also upregulated in the Cj1556 mutant, and subsequent studies showed that the mutant had a reduced ability to form biofilms. This study identified a novel C. jejuni transcriptional regulator, Cj1556, that is involved in oxidative and aerobic stress responses and is important for the survival of C. jejuni in the natural environment and in vivo .

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The iron-induced ferredoxin FdxA of Campylobacter jejuni is involved in aerotolerance

Cited by 39 publications

References 15 publications

Iron Acquisition and Regulation in Campylobacter jejuni

Iron Acquisition and Regulation in Campylobacter jejuni

Selenium-Dependent Biogenesis of Formate Dehydrogenase in Campylobacter jejuni Is Controlled by the fdhTU Accessory Genes

The Campylobacter jejuni Transcriptional Regulator Cj1556 Plays a Role in the Oxidative and Aerobic Stress Response and Is Important for Bacterial SurvivalIn Vivo

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