Tobias Bergmiller | Biosciences | University of Exeter

Dr Tobias Bergmiller

Lecturer

T.Bergmiller2@exeter.ac.uk

5160

+44 01392 725160

Living Systems Institute T04. 09

Living Systems Institute, University of Exeter, Stocker Road, Exeter, EX4 4QD

Overview

Quantitative Single-Cell Microbiology

My lab works at a broad range of topics that touch on synthetic biology, antibiotic resistance and phage biology. We are using a suite of quantitative tools including bespoke fluorescence microscopy and microfluidics.

Physiological effects of sub-inhibitory antibiotic concentrations on bacteria

Antibotic resistant bacteria are of global concern. Bacteria frequently encounter low and sub-inhibitory (sub-MIC) antibiotic concentrations either in nature by anthropogenic emissions or during treatment. We are specifically interested in the interplay between bacterial physiology such as growth and gene expression and sub-MIC antibiotics.

Synthetic Biology and Bacterial Devices

We are interested in using latest synthetic biology tools to control biological systems in order to investigate biological processes. This includes the development of new bacterial devices and technology for live-cell imaging.

Biography

Tobias Bergmiller joined the Living Systems Institute in February 2019 as Lecturer in Biosciences. He gained his PhD at ETH Zurich in Microbial Ecology and Evolution and did his PostDoc at IST Austria in Vienna.

Qualifications

2005-2011 PhD (Molecular Microbial Ecology and Evolution) ETH Zurich, Switzerland

1999 – 2005 Diploma/Masters (Microbiology) University of Constance, Germany

Career

2019 – present Lecturer in Biosciences, University of Exeter

2018 Parental leave

2011 – 2017 PostDoc, IST Austria

Research group links

Research

Research interests

Phenotypic Heterogeneity and Adaptive Responses in Bacteria

Binary fission of rod-shaped bacteria results in virtually identical sibling cells, which consist of the same genetic makeup. Despite of being extremely similar, such clonal sibling cells can differ from each other phenotypically and consequently display distinct behaviors. Unequal or biased partitioning of cellular constituents at cell division is one non-exclusive, yet little understood mechanism that can generate such phenotypic heterogeneity. My work is focused on directional inheritance of cell structures leading to non-random variability in basic traits or determination of cell fate, such as cell size, live span or response to antibiotics. My recent work focuses on partitioning of multi-drug efflux pumps in Escherichia coli, which are large trans-membrane- and trans-envelope protein structures that are at the core of innate resistance to many classes of antibiotics, thus complicating antibiotic treatment. Here, biased partitioning results in different degrees of antibiotic tolerance in individual cell lineages. To elucidate the molecular mechanisms that underlie partitioning, I investigate translation of trans-membrane proteins and complex assembly at the subcellular level.

Research projects

Partitioning of Multi-Drug Efflux pumps and its consequences for bacterial phenotypic heterogeneity
Sub-cellular organization of trans-membrane protein translation and protein complex assembly
Bacterial adaptation to low antibiotic concentrations

Publications

Journal articles

Beardmore R, Gudelj I, Reding C, Wood E, Bergmiller T, Schulenberg H, Philip R, Catalan P (In Press). The Antibiotic Dosage of Fastest Resistance Evolution: gene amplifications underpinning the inverted-U. Molecular Biology and Evolution

Wood E, Schulenburg H, Rosenstiel P, Bergmiller T, Ankrett D, Gudelj I, Beardmore R (2023). Ribosome-binding antibiotics increase bacterial longevity and growth efficiency. Proc Natl Acad Sci U S A, 120(40). Abstract. Author URL.

Reding C, Hewlett M, Bergmiller T, Gudelj I, Beardmore R (2019). Fluorescence photography of patterns and waves of bacterial adaptation at high antibiotic doses. Abstract.

Nikolic N, Bergmiller T, Vandervelde A, Albanese TG, Gelens L, Moll I (2018). Autoregulation of mazEFexpression underlies growth heterogeneity in bacterial populations. Nucleic Acids Research, 46(6), 2918-2931. Abstract.

Tomasek K, Bergmiller T, Guet CC (2018). Lack of cations in flow cytometry buffers affect fluorescence signals by reducing membrane stability and viability of Escherichia coli strains. Journal of Biotechnology, 268, 40-52. Abstract.

De Martino D, MC Andersson A, Bergmiller T, Guet CC, Tkačik G (2018). Statistical mechanics for metabolic networks during steady state growth. Nature Communications, 9(1). Abstract.

Renault TT, Abraham AO, Bergmiller T, Paradis G, Rainville S, Charpentier E, Guet CC, Tu Y, Namba K, Keener JP, et al (2017). Bacterial flagella grow through an injection-diffusion mechanism. eLife, 6 Abstract.

Bergmiller T, Andersson AMC, Tomasek K, Balleza E, Kiviet DJ, Hauschild R, Tkačik G, Guet CC (2017). Biased partitioning of the multidrug efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity. Science, 356(6335), 311-315. Abstract.

Nikolic N, Schreiber F, Dal Co A, Kiviet DJ, Bergmiller T, Littmann S, Kuypers MMM, Ackermann M (2017). Cell-to-cell variation and specialization in sugar metabolism in clonal bacterial populations. PLoS Genetics, 13(12). Abstract.

Chait R, Ruess J, Bergmiller T, Tkačik G, Guet CC (2017). Shaping bacterial population behavior through computer-interfaced control of individual cells. Nature Communications, 8(1). Abstract.

Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR (2016). Adaptation to parasites and costs of parasite resistance in mutator and nonmutator bacteria. Molecular Biology and Evolution, 33(3), 770-782. Abstract.

Pleška M, Qian L, Okura R, Bergmiller T, Wakamoto Y, Kussell E, Guet CC (2016). Bacterial autoimmunity due to a restriction-modification system. Current Biology, 26(3), 404-409. Abstract.

Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M (2016). Genetic Manipulation of Glycogen Allocation Affects Replicative Lifespan in E. coli. PLoS Genetics, 12(4). Abstract.

Dhar R, Bergmiller T, Wagner A (2014). Increased gene dosage plays a predominant role in the initial stages of evolution of duplicate tem-1 beta lactamase genes. Evolution, 68(6), 1775-1791. Abstract.

Refardt D, Bergmiller T, Kümmerli R (2013). Altruism can evolve when relatedness is low: Evidence from bacteria committing suicide upon phage infection. Proceedings of the Royal Society B: Biological Sciences, 280(1759). Abstract.

Bergmiller T, Ackermann M, Silander OK (2012). Patterns of evolutionary conservation of essential genes correlate with their compensability. PLoS Genetics, 8(6). Abstract.

Bergmiller T, Ackermann M (2011). Pole age affects cell size and the timing of cell division in Methylobacterium extorquens AM1. Journal of Bacteriology, 193(19), 5216-5221. Abstract.

Bergmiller T, Peña-Miller R, Boehm A, Ackermann M (2011). Single-cell time-lapse analysis of depletion of the universally conserved essential protein YgjD. BMC Microbiol, 11 Abstract. Author URL.

Dippel R, Bergmiller T, Böhm A, Boos W (2005). The maltodextrin system of Escherichia coli: Glycogen-derived endogenous induction and osmoregulation. Journal of Bacteriology, 187(24), 8332-8339. Abstract.