A co-conserved gene pair supports Caulobacter iron homeostasis and resistance to chelation stress
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ABSTRACT:
PROVIDER: PRJNA1145551 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30167052_1.fastq.gz | Fastqsanger.gz | |||
| SRR30167052_2.fastq.gz | Fastqsanger.gz | |||
| SRR30167053_1.fastq.gz | Fastqsanger.gz | |||
| SRR30167053_2.fastq.gz | Fastqsanger.gz | |||
| SRR30167054_1.fastq.gz | Fastqsanger.gz |
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Project description:Bacteria assimilate a diverse set of metals that enable metabolic functions essential for growth and survival, but metal homeostasis can be disrupted by natural and synthetic chelators in the environment. We have identified genes that influence fitness of the common soil and aquatic bacterium, Caulobacter crescentus, in the presence of a growth-limiting concentration of the synthetic chelator ethylenediaminetetraacetic acid (EDTA). Among the identified genes important in EDTAacclimationthere are several controlled by the metal-responsive regulators Fur, Zur, and UzcRS. However, a subset of genes in the iron-responsive Fur regulon emerged as the primary fitness determinants during EDTA challenge. EDTA treatment reduced intracellular iron levels and a syntenic gene pair, cciT and cciO, that supports Caulobacter iron homeostasis is necessary for growth in EDTA. cciT encodes one of four Fur-regulated TonB-dependent transporters (TBDTs) and – of these regulators – uniquely supports wild-type levels of growth on defined and complex lab media. The iron acquisition and EDTA resistance functions of the CciT transporter specifically require the presence of cciO, which encodes a 2-oxoglutarate-Fe(II) dioxygenase. Thus, there is a critical functional partnership between an outer membrane transporter and a cytoplasmic dioxygenase that are broadly co-conserved in the phylum Proteobacteria. cciT and cciO mutants cultivated in natural freshwater were not impacted by an equivalent EDTA treatment, demonstrating robustness of the highly redundant set of Caulobacter iron acquisition systems in an ecosystem context. This study advances our understanding of genes involved in metal acquisition and chelation stress survival, and illuminates the complex interactions between the chemical environment and the processes that regulate intracellular metal homeostasis.
2024-08-14 | GSE274268 | GEO
Project description:Synthetic metal chelators are widely used in industrial, clinical, and agricultural settings, leading to their accumulation in the environment. We measured the growth of Caulobacter crescentus, a soil and aquatic bacterium, in the presence of the ubiquitous chelator ethylenediaminetetraacetic acid (EDTA) and found that it restricts growth by lowering intracellular iron levels. Using barcoded transposon sequencing, we identified an operonic gene pair, cciT-cciO, that is required to maintain iron homeostasis in laboratory media during EDTA challenge. cciT encodes one of four TonB-dependent transporters that are regulated by the ferric uptake repressor (Fur) and stands out among this group of genes in its ability to support Caulobacter growth across diverse media conditions. The function of CciT strictly requires cciO, which encodes a cytoplasmic FeII dioxygenase-family protein. Our results thus define a functional partnership between an outer membrane iron receptor and a cytoplasmic dioxygenase that are broadly co-conserved in Proteobacteria. We expanded our analysis to natural environments by examining the growth of mutant strains in freshwater from two lakes, each with biochemical and geochemical profiles that differ markedly from standard laboratory media. In lake water, Caulobacter growth did not require cciT or cciO and was less affected by EDTA treatment. This result aligns with our observation that EDTA toxicity is influenced by common forms of biologically chelated iron and the spectrum of free cations present in the medium. Our study defines a conserved iron acquisition system in Proteobacteria and bridges laboratory-based physiology studies with real-world conditions.ImportanceMetal-chelating chemicals are widely used across industries, including as preservatives in the food sector, but their full impact on microbial physiology is not well understood. We identified two genes, cciT and cciO, that function together to support Caulobacter crescentus iron balance when cells are exposed to the common synthetic chelator, EDTA. CciT is an outer membrane transporter and CciO is a dioxygenase-family protein that are mutually conserved in many bacteria, including several human pathogens, where mutations in cciT homologs are linked to clinical resistance to the siderophore antibiotic, cefiderocol. This study identifies a conserved genetic system that supports iron homeostasis during chelation stress and illuminates the iron acquisition versatility and stress resilience of Caulobacter in freshwater environments.
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Project description:Iron deficiency is a highly prevalent nutrient deficiency and the most common cause of anemia. Although iron deficiency exacerbates cardiovascular disease, the direct impact of iron deficiency on the vasculature remains unstudied. Human lymphatic and arterial endothelial cells were treated with deferoxamine for 24 hours to assess the impact of iron deficiency on endothelial cell phenotypes. We found iron chelation upregulated the expression of arterial makers in both cell types. In lymphatic endothelial cells, iron chelation decreased the expression of lymphatic markers. These data suggest iron chelation shifts endothelial cells toward an arterial phenotype.
2025-12-31 | GSE314015 | GEO
Project description:Iron chelation shifts endothelial phenotypes
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Project description:Iron accumulation in cancer cells contributes to malignant progression and chemoresistance. While disrupting this process can influence various hallmarks of cancer, the immunomodulatory effects of chelating iron in tumors remain undefined. Here, we report that treatment with deferiprone, an FDA-approved iron chelator, elicits innate immune responses that control metastatic ovarian cancer. Deferiprone reprogrammed ovarian cancer cells towards an immunostimulatory state characterized by enhanced production of type I interferon (IFN) and surface overexpression of molecules that activate natural killer (NK) cells. Mechanistically, this reprogramming was driven by innate sensing of mitochondrial DNA in the cytosol and concomitant activation of nuclear DNA damage responses evoked upon iron chelation. Deferiprone administration synergized with chemotherapy and prolonged the survival of mice bearing metastatic ovarian cancer by bolstering intratumoral NK cell infiltration and type I IFN responses. Iron chelation may represent an alternative immunotherapeutic approach for malignancies that are normally refractory to T cell-centric modalities.
2024-06-26 | GSE246051 | GEO
Project description:Change expression of genes in iron chelation and deficient conditions
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Project description:Caulobacter sp. YL-Caulobacter Genome sequencing
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Project description:Iron chelation therapy elicits innate immune control of metastatic ovarian cancer
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Project description:This SuperSeries is composed of the following subset Series: GSE25996: Expression data from Caulobacter crescentus starved for carbon GSE25997: Expression data from Caulobacter crescentus (syn. C. vibrioides) swarmer and stalked cells starved for carbon GSE25998: Expression data from WT, DSigT and DSigU Caulobacter crescentus (syn. C. vibrioides) starved for carbon Refer to individual Series
2011-04-20 | E-GEOD-25999 | biostudies-arrayexpress
Project description:Investigation of whole genome gene expression level changes in a Caulobacter crescentus NA1000 delta-CCNA_00382 (ccrM) mutant, compared to the wild-type strain. The mutations engineered into this strain render it incapable of methylating its genome on the adenine at GANTC motifs. References for strains : WT: Marks, M.E., Castro-Rojas, C.M., Teiling, C., Du, L., Kapatral, V., Walunas, T.L. and Crosson, S. (2010) The genetic basis of laboratory adaptation in Caulobacter crescentus. J Bacteriol, 192, 3678-3688; Collier, J. and Shapiro, L. (2009) Feedback control of DnaA-mediated replication initiation by replisome-associated HdaA protein in Caulobacter. J Bacteriol, 191, 5706-5716. DccrM: Gonzalez, D. and Collier, J. (2013) DNA methylation by CcrM activates the transcription of two genes required for the division of Caulobacter crescentus. Mol Microbiol, 88, 203-218. A six chip study using total RNA recovered from three separate wild-type cultures of Caulobacter crescentus NA1000 and three separate cultures of a triple mutant strain, Caulobacter crescentus NA1000 delta-CCNA_00382 (ccrM), in which the ccrM gene coding for a DNA methyltransferase methylating the adenine in GANTC motifs is truncated and its product inactive. Each chip measures the expression level of 3933 genes from Caulobacter crescentus NA1000 with 3 probes per gene and with three-fold technical redundancy.
2014-01-08 | E-GEOD-52375 | biostudies-arrayexpress