Browse by author
Lookup NU author(s): Dr Jacob BiboyORCiD, Dr Daniela Vollmer, Professor Waldemar Vollmer
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
© 2024 by the authors.Bicarbonate and CO2 are essential substrates for carboxylation reactions in bacterial central metabolism. In Staphylococcus aureus, the bicarbonate transporter, MpsABC (membrane potential-generating system) is the only carbon concentrating system. An mpsABC deletion mutant can hardly grow in ambient air. In this study, we investigated the changes that occur in S. aureus when it suffers from CO2/bicarbonate deficiency. Electron microscopy revealed that ΔmpsABC has a twofold thicker cell wall thickness compared to the parent strain. The mutant was also substantially inert to cell lysis induced by lysostaphin and the non-ionic surfactant Triton X-100. Mass spectrometry analysis of muropeptides revealed the incorporation of alanine into the pentaglycine interpeptide bridge, which explains the mutant’s lysostaphin resistance. Flow cytometry analysis of wall teichoic acid (WTA) glycosylation patterns revealed a significantly lower α-glycosylated and higher ß-glycosylated WTA, explaining the mutant’s increased resistance towards Triton X-100. Comparative transcriptome analysis showed altered gene expression profiles. Autolysin-encoding genes such as sceD, a lytic transglycosylase encoding gene, were upregulated, like in vancomycin-intermediate S. aureus mutants (VISA). Genes related to cell wall-anchored proteins, secreted proteins, transporters, and toxins were downregulated. Overall, we demonstrate that bicarbonate deficiency is a stress response that causes changes in cell wall composition and global gene expression resulting in increased resilience to cell wall lytic enzymes and detergents.
Author(s): Liberini E, Fan S-H, Bayer AS, Beck C, Biboy J, Francois P, Gray J, Hipp K, Koch I, Peschel A, Sailer B, Vollmer D, Vollmer W, Gotz F
Publication type: Article
Publication status: Published
Journal: International Journal of Molecular Sciences
Year: 2024
Volume: 25
Issue: 17
Print publication date: 01/09/2024
Online publication date: 26/08/2024
Acceptance date: 19/08/2024
Date deposited: 25/09/2024
ISSN (print): 1661-6596
ISSN (electronic): 1422-0067
Publisher: Multidisciplinary Digital Publishing Institute (MDPI)
URL: https://doi.org/10.3390/ijms25179251
DOI: 10.3390/ijms25179251
Data Access Statement: Raw expression data for these samples were submitted to the ENA database under project accession number PRJEB65327.
PubMed id: 39273203
Altmetrics provided by Altmetric
