1) Gene amplification causes prokaryotic heterogeneity.
Gene duplication and amplification (GDA) is a RecA-dependent genetic process allowing the creation of gene arrays (identical copies of genes in a repeated fashion). These arrays are able to expand and contract in an accordion-like fashion and create bacterial siblings with unique characteristics. Little is known about the frequency of duplications in clinical populations of pathogens and the importance of the mechanism to influence the success of a lineage during colonization or during invasive disease is unclear.
We found that the GDA of a haem acquisition system in Staphylococcus lugdunensis transfers a competitive advantage to the lineage to thrive on haem as sole source of nutrient iron. This shows how GDAs can help to overcome selective pressures build up by our immune system. Similarly, GDAs are frequent in clinical isolates of the invasive pathogen Staphylococcus aureus and can create bacterial siblings with different immunostimulatory capacity. This shows that GDAs can impact host-pathogen interactions.
2) Competition for nutritional iron in microbial communities.
Iron is an essential trace element that needs to be acquired by all living organisms. Bacteria use small iron-binding siderophores to solubilize Fe-ions to increase biological availability. We find that harmless commensals consuming pathogen-derived siderophores can reduce the expansion of pathogens by limiting iron availability. These finding suggests that pathogens can be excluded from human microbiomes by introduction of siderophore consumers, a new strategy to prevent colonisation and infection by antibiotic resistant pathogens.
Simon Heilbronner studied Biology with microbiology as major and immunology as minor subject in Tübingen (Germany) and Uppsala (Sweden). Having gained the Diploma he went to Ireland to work in the lab of Prof. Timothy J. Foster in Trinity College Dublin (TCD) where he earned his PhD-degree in 2014. Supported by an individual Marie Skłodowska-Curie fellowship he moved back to Germany. He is leading an independent research group in the department of Infection Biology since 2018.
- European Commission for Research and Innovation – Gen Duplication and Amplification in Staphylococcal Populations. Individual Marie Skłodowska -Curie fellowship (2015-2017)
- Ministerium für Wissenschaft, Forschung und Kunst Baden-Württemberg - RiSC-Program - Detection and Effects Of Gene Amplification In Staphylococcal Clonal Populations (2018-2019)
- DFG – HE8381 - An ECF-type transporter scavenges heme to overcome iron-limitation in Staphylococcus lugdunensis
- DFG – TRR261 – Cellular Mechanism of Antibiotic Action and Production – Project B04 (https://uni-tuebingen.de/forschung/forschungsschwerpunkte/sfb-transregios/sfb-trr-antibiotic-cellmap/)
- Cluster of Excellence - Controlling Microbes to Fight Infection (https://uni-tuebingen.de/en/research/core-research/cluster-of-excellence-cmfi/cmfi/)