Bacterial Homologs of Progestin and AdipoQ Receptors (PAQRs) Affect Membrane Energetics Homeostasis but Not Fluidity

Autor: Maddison V. Melchionna, Jessica M. Gullett, Emmanuelle Bouveret, Him K. Shrestha, Paul E. Abraham, Robert L. Hettich, Gladys Alexandre
Přispěvatelé: The University of Tennessee [Knoxville], Adaptation au stress et Métabolisme chez les entérobactéries - Stress adaptation and metabolism in enterobacteria (SAMe), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Oak Ridge National Laboratory [Oak Ridge] (ORNL), UT-Battelle, LLC, This research is supported by National Science Foundation grant NSF-MCB 1715185 (to R.L.H. and G.A.), National Science Foundation grant NSF-IOS 1855066 (to G.A.), a Dr. Donald L. Akers, Jr., Faculty Enrichment award (to G.A.), and a UT research seed award (to G.A.).
Rok vydání: 2022
Předmět:
Zdroj: Journal of Bacteriology
Journal of Bacteriology, 2022, 204 (4), ⟨10.1128/jb.00583-21⟩
ISSN: 1098-5530
0021-9193
DOI: 10.1128/jb.00583-21⟩
Popis: International audience; Membrane potential homeostasis is essential for cell survival. Defects in membrane potential lead to pleiotropic phenotypes, consistent with the central role of membrane energetics in cell physiology. Homologs of the progestin and AdipoQ receptors (PAQRs) are conserved in multiple phyla of Bacteria and Eukarya. In eukaryotes, PAQRs are proposed to modulate membrane fluidity and fatty acid (FA) metabolism. The role of bacterial homologs has not been elucidated. Here, we use Escherichia coli and Bacillus subtilis to show that bacterial PAQR homologs, which we name "TrhA," have a role in membrane energetics homeostasis. Using transcriptional fusions, we show that E. coli TrhA (encoded by yqfA) is part of the unsaturated fatty acid biosynthesis regulon. Fatty acid analyses and physiological assays show that a lack of TrhA in both E. coli and B. subtilis (encoded by yplQ) provokes subtle but consistent changes in membrane fatty acid profiles that do not translate to control of membrane fluidity. Instead, membrane proteomics in E. coli suggested a disrupted energy metabolism and dysregulated membrane energetics in the mutant, though it grew similarly to its parent. These changes translated into a disturbed membrane potential in the mutant relative to its parent under various growth conditions. Similar dysregulation of membrane energetics was observed in a different E. coli strain and in the distantly related B. subtilis. Together, our findings are consistent with a role for TrhA in membrane energetics homeostasis, through a mechanism that remains to be elucidated.
Databáze: OpenAIRE