We study different molecular mechanisms relevant for understanding antibiotic resistance and for identification of novel antimicrobial target sites in pneumococci (pneumokokker, S. pneumoniae) and staphylococci (stafylokokker, S. aureus). These pathogens are responsible for millions of deaths worldwide every year and treatment of infections are increasingly problematic due to the emergence and spread of antibiotic resistance (including penicillin-resistant S. pneumoniae and methicillin-resistant S. aureus, MRSA).
News & new publications
- June 2018: Nascent teichoic acids insertion into the cell wall directs the localization and activity of the major pneumococcal autolysin LytA, published in The Cell Surface.
- June 2018: Our paper on S. aureus cell division (CozEa and CozEb play overlapping and essential roles in controlling cell division in Staphylococcus aureus), is now published in Molecular Microbiology.
- June 2018: Crosstalk and eavesdropping among quorum sensing peptide signals that regulate bacteriocin production in Streptococcus pneumoniae, published in ISME J.
- Oct 2017: Quorum-sensing integrates environmental cues, cell density and cell history to control bacterial competence published in Nature Communications.
- July 2017: Identification of EloR as a regulator of cell elongation in Streptococcus pnumoniae published in Molecular Microbiology.
Main research topics
Bacterial transformation and quorum sensing
Transformation by horizontal gene transfer has been an underestimated factor in the evolution of life on earth. For example, the rapid emergence of penicillin resistance among pneumococcal strains is due to their natural ability to become competent for natural transformation, i.e. to take up naked DNA from the environment. This property enables pneumococci to exchange genes with their siblings or members of closely related species. To be able to control the spread of antibiotic resistance and other virulence genes it is important to understand how natural transformation contributes to the dissemination of these genes.
Natural transformation in pneumococci also represents a prominent example of quorum sensing based gene regulation, where bacteria communicate via export of small peptide pheromones. The group aims at understand the molecular details of such quorum sensing based gene regultaion and eventually be able to control such mechanisms.
Penicillin resistance and cell wall synthesis in Streptococcus pneumoniae
The cellular targets of penicillins are the so called penicillin-binding proteins (PBPs). Alterations in these enzymes that reduce their affinity for penicillins have been recognized as the major penicillin-resistance mechanism operating in S. pneumoniae. The normal function of PBPs is to synthesize the pneumococcal cell wall (the peptidoglycan sacculus). Although the reactions catalyzed by the pneumococcal PBPs are well known, there are several aspects related to PBPs which are poorly understood. We are therefore studying (i) the specific role of each PBP in synthesizing and shaping the peptidoglycan sacculus, (ii) regulation of PBP activity (iii) interaction between PBPs and other proteins, (iv) sub-cellular localization of PBPs and the activities of low-affinity PBPs.
The cell cycle of Staphylococcus aureus
Many antibiotics are targeting essential processes of the bacterial cell cycle, including DNA replication, cell wall synthesis and cell division. Using different genetics and biochemistry approaches, we aim to identify novel factors involved in the staphylococcal cell cycle, which can serve as target sites for antimicrobials.
Catharina S. Heiland, master student