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The SPFH complex HflK-HflC regulates aerobic respiration in bacteria

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Pérez-López,  Maria Isabel
Microbial Networks, Department of Systems and Synthetic Microbiology, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Angelidou,  Georgia
Core Facility Mass Spectrometry and Proteomics, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;
Core Facility Metabolomics and small Molecules Mass Spectrometry, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Glatter,  Timo       
Core Facility Mass Spectrometry and Proteomics, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Paczia,  Nicole       
Core Facility Metabolomics and small Molecules Mass Spectrometry, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Sourjik,  Victor       
Microbial Networks, Department of Systems and Synthetic Microbiology, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Citation

Pérez-López, M. I., Lubrano, P., Angelidou, G., Glatter, T., Paczia, N., Link, H., et al. (2024). The SPFH complex HflK-HflC regulates aerobic respiration in bacteria. bioRxiv: the preprint server for biology, 2024.04.21.590321.


Cite as: https://hdl.handle.net/21.11116/0000-000F-300C-E
Abstract
The bacterial HflK-HflC membrane complex is a member of the highly conserved SPFH protein family, which is found throughout all domains of life and includes eukaryotic stomatins, flotillins, and prohibitins. These proteins organize cell membranes and are involved in various processes. However, the exact physiological functions of most bacterial SPFH proteins remain unclear. Here, we report that the HflK-HflC complex in Escherichia coli is required for growth under high aeration. The absence of this complex causes an aerobic growth defect due to a reduced abundance of IspG, a crucial enzyme in the isoprenoid biosynthetic pathway. This reduction leads to lower levels of ubiquinone, reduced respiration, lower ATP levels, and misregulated expression of respiratory genes. The regulation of aerobic respiration by the HflK-HflC complex resembles the mitochondrial respiratory defects caused by prohibitin mutations in mammalian and yeast cells, suggesting a functional commonality between these bacterial and eukaryotic SPFH proteins.Competing Interest StatementThe authors have declared no competing interest.