Methylotuvimicrobium buryatense strain:5GB1C
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA515283 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Methylotuvimicrobium buryatense strain:5GB1C Transcriptome or Gene expression
| PRJNA720552 | ENA
Project description:Methylomicrobium buryatense 5GB1C resequencing
| PRJNA322692 | ENA
Project description:Functional genomics of Methylotuvimicrobium buryatense
| PRJNA718747 | ENA
Project description:Functional genomics of Methylomicrobium buryatense
| PRJNA718760 | ENA
Project description:Methylotuvimicrobium buryatense 5G strain:5G Genome sequencing and assembly
| PRJNA89087 | ENA
Project description:The bacteria that grow on methane aerobically (methanotrophs) support populations of non-methanotrophs in the natural environment by excreting methane-derived carbon. One group of excreted compounds are short-chain organic acids, generated in highest abundance when cultures are grown under O2-starvation. We examined this O2-starvation condition in the methanotroph Methylomicrobium buryatense 5GB1C . Under prolonged O2-starvation in a closed vial, this methanotroph increases the amount of acetate excreted about 10-fold, but the formate, lactate, and succinate excreted do not respond to this culture condition. In bioreactor cultures, the amount of each excreted product is similar across a range of growth rates and limiting substrates, including O2-limitation. A set of mutants were generated in genes predicted to be involved in generating or regulating excretion of these compounds and tested for growth defects, and changes in excretion products. The phenotypes and associated metabolic flux modeling suggested that in M. buryatense 5GB1C, formate and acetate are excreted in response to redox imbalance, and the resulting metabolic state represents a combination of fermentation and respiration metabolism.
2017-08-24 | GSE101981 | GEO
Project description:OXYGEN-LIMITED METABOLISM IN THE METHANOTROPH METHYLOMICROBIUM BURYATENSE 5GB1C
| PRJNA396065 | ENA
Project description:Several of the metabolic enzymes in methanotrophic bacteria rely on metals for both their expression and their catalysis. The MxaFI methanol dehydrogenase enzyme complex uses calcium as a cofactor to oxidize methanol, while the alternative methanol dehydrogenase XoxF uses lanthanide metals such as lanthanum and cerium for the same function. Lanthanide metals, abundant in the earth’s crust and widely used in electronic devices, strongly repress the transcription of mxaF yet activate the transcription of xoxF. This phenomenon of mxaF repression and xoxF activation in the presence of lanthanides is called the “lanthanide switch.” To better understand components of the lanthanide switch in the Type I gammaproteobacterial methanotroph “Methylotuvimicrobium buryatense” 5GB1C, we designed a mutagenesis system and selected for mutants unable to repress the mxaF promoter in the presence of lanthanum. Whole genome resequencing for multiple lanthanide switch mutants identified several unique point mutations in a single gene encoding a TonB-dependent receptor, which we have named LanA. While the LanA TonB-dependent receptor is absolutely required for the lanthanide switch, it does not affect lanthanum uptake by the bacterium. Deletion of a separate lanthanide-repressible gene encoding a TonB protein had no effect on the lanthanide switch or on lanthanum uptake. The discovery of this novel component of the lanthanide regulatory system highlights the complexity of this circuit and suggests further components are likely involved.
2019-05-21 | GSE125909 | GEO
Project description:Methylomicrobium buryatense overview
| PRJNA89363 | ENA
Project description:Methylotuvimicrobium buryatense 5GB1C, a fast-growing gammaproteobacterial methanotroph, is equipped with two glycolytic pathways, the Entner-Doudoroff (ED) pathway and the Embden-Meyerhof-Parnas (EMP) pathway. Metabolic flux analysis and 13C-labeling experiments have shown the EMP pathway is the principal glycolytic route in M. buryatense 5GB1C, while the ED pathway appears to be metabolically and energetically insignificant. However, it has not been possible to obtain a null mutant in the edd-eda genes encoding the two unique enzymatic reactions in the ED pathway, suggesting the ED pathway may be essential for M. buryatense 5GB1C growth. In this study, the inducible P BAD promoter was used to manipulate gene expression of edd-eda, and in addition, the expression of these two genes was separated from that of a downstream gltA gene. The resulting strain shows arabinose-dependent growth that correlates with ED pathway activity, with normal growth achieved in the presence of ∼0.1 g/liter arabinose. Flux balance analysis shows that M. buryatense 5GB1C with a strong ED pathway has a reduced energy budget, thereby limiting the mutant growth at a high concentration of arabinose. Collectively, our study demonstrates that the ED pathway is essential for M. buryatense 5GB1C. However, no known mechanism can directly explain the essentiality of the ED pathway, and thus, it may have a yet unknown regulatory role required for sustaining a healthy and functional metabolism in this bacterium.IMPORTANCE The gammaproteobacterial methanotrophs possess a unique central metabolic architecture where methane and other reduced C1 carbon sources are assimilated through the ribulose monophosphate cycle. Although efforts have been made to better understand methanotrophic metabolism in these bacteria via experimental and computational approaches, many questions remain unanswered. One of these is the essentiality of the ED pathway for M. buryatense 5GB1C, as current results appear contradictory. By creating a construct with edd-eda and gltA genes controlled by P BAD and P J23101 , respectively, we demonstrated the essentiality of the ED pathway for this obligate methanotroph. It is also demonstrated that these genetic tools are applicable to M. buryatense 5GB1C and that expression of the target genes can be tightly controlled across an extensive range. Our study adds to the expanding knowledge of methanotrophic metabolism and practical approaches to genetic manipulation for obligate methanotrophs.
| S-EPMC7848903 | biostudies-literature