Background: Sulfate-reducing bacteria (SRB) drive the ocean sulfur and carbon cycling. They constitute a diverse phylogenetic and physiological group and are widely distributed in anoxic marine environments. From a physiological viewpoint, SRB's can be categorized as complete or incomplete oxidizers, meaning that they either oxidize their carbon substrate completely to CO or to a stoichiometric mix of CO and acetate. Members of Desulfofabaceae family are incomplete oxidizers, and within that family, Desulfofaba is the only genus with three isolates that are classified into three species. Previous physiological experiments revealed their capability of respiring oxygen.
Results: Here, we sequenced the genomes of three isolates in Desulfofaba genus and reported on a genomic comparison of the three species to reveal their metabolic potentials. Based on their genomic contents, they all could oxidize propionate to acetate and CO. We confirmed their phylogenetic position as incomplete oxidizers based on dissimilatory sulfate reductase (DsrAB) phylogeny. We found the complete pathway for dissimilatory sulfate reduction, but also different key genes for nitrogen cycling, including nitrogen fixation, assimilatory nitrate/nitrite reduction, and hydroxylamine reduction to nitrous oxide. Their genomes also contain genes that allow them to cope with oxygen and oxidative stress. They have genes that encode for diverse central metabolisms for utilizing different substrates with the potential for more strains to be isolated in the future, yet their distribution is limited.
Conclusions: Results based on marker gene search and curated metagenome assembled genomes search suggest a limited environmental distribution of this genus. Our results reveal a large metabolic versatility within the Desulfofaba genus which establishes their importance in biogeochemical cycling of carbon in their respective habitats, as well as in the support of the entire microbial community through releasing easily degraded organic matters.
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http://dx.doi.org/10.1186/s12864-023-09297-2 | DOI Listing |
iScience
January 2025
Department of Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ocul Surf
December 2024
The First Hospital Affiliated to Heilongjiang University of Chinese Medicine, Harbin, 150040, China. Electronic address:
Dry eye disease (DED) is a multifactorial condition with complex and incompletely understood molecular mechanisms. Advances in multi-omics technologies, including genomics, transcriptomics, proteomics, metabolomics, and microbiomics, have provided new insights into the pathophysiology of DED. Genomic analyses have identified key genetic variants linked to immune regulation and lacrimal gland function.
View Article and Find Full Text PDFmSphere
December 2024
Department of Chemical and Biomolecular Engineering, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.
During aerobic growth, relies on acetate overflow metabolism, a process where glucose is incompletely oxidized to acetate, for its bioenergetic needs. Acetate is not immediately captured as a carbon source and is excreted as waste by cells. The underlying factors governing acetate overflow in have not been identified.
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January 2025
Department of General Practice, Yantaishan Hospital Affiliated to Binzhou Medical University, Yantai, China.
Introduction: Persistent postural-perceptual dizziness (PPPD) is the most prevalent chronic functional dizziness in the clinic. Unsteadiness, dizziness, or non-spinning vertigo are the main symptoms of PPPD, and they are typically aggravated by upright posture, active or passive movement, and visual stimulation. The pathogenesis of PPPD remains incompletely understood, and it cannot be attributed to any specific anatomical defect within the vestibular system.
View Article and Find Full Text PDFRedox Biol
December 2024
Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA, USA; Department of Biomedical Engineering, UAB, Birmingham, AL, USA. Electronic address:
Background: Diabetes increases ischemic heart injury via incompletely understood mechanisms. We recently reported that diabetic adipocytes-derived small extracellular vesicles (sEV) exacerbate myocardial reperfusion (MI/R) injury by promoting cardiomyocyte apoptosis. Combining in vitro mechanistic investigation and in vivo proof-concept demonstration, we determined the underlying molecular mechanism responsible for diabetic sEV-induced cardiomyocyte apoptosis after MI/R.
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