Leise Riber

Leise Riber


Research interests

My main focus is on finding new strategies to limit the occurrence of plasmid-borne spread of antimicrobial resistance. The spread of antimicrobial resistance among bacterial populations is mainly due to the acquisition of resistance genes located on transferable plasmids obtained through horizontal gene transfer. New ways of reducing the spread and selection of resistance therefore include the disturbance of the dynamics of plasmid transfer and stability. Current work areas include studying molecular mechanisms involved in horizontal gene transfer and plasmid stability, as well as baseline studies of the prevalence and dissemination of resistance plasmids in complex natural environments. Areas of expertise include various techniques within molecular microbiology and bacterial genetics. Main focus is on construction of bacterial reporter strains and cloning of conjugative plasmids using mini-mu and Tn7 based transposon systems for studies of horizontal gene transfer (HGT) and plasmid dynamics in complex environments. Additionally, HGT studies include expertise within cell counting using flow cytometry as well as cell sorting for 16S sequencing using Fluorescence activated cell sorting (FACS).


2003-2007 Ph.D., (Molecular Microbiology). Roskilde University, Roskilde.

1996-2003  Cand. Polyt., (Chemistry, Biotechnology). Technical University of Denmark, Lyngby.


2010-        Post-doctoral Fellow, (Molecular Microbiology). University of Copenhagen, Institute of Biology, KU-BIO, Copenhagen.

2008-2010 Post-doctoral Fellow, (Molecular Microbiology and Food Microbiology). National Food Institute, Technical University of Denmark, DTU-FOOD, Mørkhøj.

2006-2007   Post-doctoral Fellow, (Molecular Microbiology). Roskilde University, Roskilde.

Publications and Presentations

5 publications in international peer reviewed journals; about 10 contributions to

conferences (posters, oral presentations), workshops, etc. Once receiver of the

Scholarship “Carlsbergs Mindelegat for Brygger J.C. Jacobsen”.


1.         Charbon, G., et al., Suppressors of DnaA(ATP) imposed overinitiation in Escherichia coli. Mol Microbiol. 2011. 79(4): p. 914-28.

2.         Gronlund, H., et al., Microarray-based genotyping of Salmonella: inter-laboratory evaluation of reproducibility and standardization potential. Int J Food Microbiol. 2011. 145: p. S79-85.

3.         Riber, L., et al., Loss of Hda activity stimulates replication initiation from I-box, but not R4 mutant origins in Escherichia coli. Mol Microbiol, 2009. 71(1): p. 107-22.

4.         Riber, L. and A. Lobner-Olesen, Coordinated replication and sequestration of oriC and dnaA are required for maintaining controlled once-per-cell-cycle initiation in Escherichia coli. J Bacteriol, 2005. 187(16): p. 5605-13.

5.         Riber, L., et al., Hda-mediated inactivation of the DnaA protein and dnaA gene autoregulation act in concert to ensure homeostatic maintenance of the Escherichia coli chromosome. Genes Dev, 2006. 20(15): p. 2121-34.


Cand polyt, PhD

ID: 17515397