Frederic Bertels

Research Group Leader
Affiliated projects

I started my scientific career in Jena where I studied bioinformatics. I then went on to write my Diploma thesis at the German Cancer Research Center in Heidelberg, which I wrote on protein function prediction based on secondary structure comparison. After I finished my thesis work, I decided to get to know the world and continued doing science in a gap year in Auckland, New Zealand. In Auckland I started working in the Bioinformatics Institute with Allen Rodrigo on inferring phylogenies from metagenomic sequencing data (Rodrigo et al. 2008). I then went on to work with Justin O’Sullivan on predicting the three dimensional structure of the yeast genome (Rodley et al. 2009).

After having spent almost a year in Auckland, I met Paul for the first time at Massey University in Auckland. Paul and I got along well enough for him to offer me a PhD position in his lab and I started working on repetitive sequences in the P. fluorescens SBW25 genome. During my PhD I discovered that REPINs are the replicative unit REP sequences are organized in (Bertels and Rainey 2011aBertels and Rainey 2011b) and that a single copy transposase is responsible for the dissemination of REPINs inside the genome (Bertels et al. 2017a). I also worked on a range of other exciting projects that Paul and other lab members needed computational support with.

After my PhD I went on to do a PostDoc at the Biozentrum in Basel under the supervision of Erik van Nimwegen and Olin Silander. In Basel I learned a lot about bacterial phylogenetic trees and how to build them (Bertels et al. 2014).

After about 2.5 years I went on to do my second PostDoc with Roland Regoes at the ETH Zurich. Roland and I worked on the evolution of HIV, which was my first exposure to the evolution of viruses (Bertels et al. 2018Bons et al. 2018Bertels et al. 2018Bertels et al. 2019). Although I am not working on HIV anymore, I am still very much interested in virus evolution and decided to use a more tractable experimental system of PhiX174 infecting E. coli C. My first (very talented!) PhD student Jordan Romeyer Dherbey is currently investigating how E. coli C becomes resistant to PhiX174 and how PhiX174 can overcome this resistance.

In 2015 I started a PostDoc with Arne Traulsen in the Department of Evolutionary Theory here at the Max Planck Institute in Plön. Together with Arne and Chaitanya Gokhale, I worked on inferring REPIN duplication rates (Bertels et al. 2017b). This was the first time we took advantage of the fact that REPINs are sequence populations to learn something about REPIN population dynamics.

In June 2017 I started my current position as the group leader of the Microbial Molecular Evolution lab. We are interested in learning about phage evolution and REPIN/RAYT evolution and ecology. Here is a link to my group website.

Research interests

Evolution and ecology of intragenomic sequence populations (REPIN and RAYTs in particular).

Phage and virus evolution.

Bacterial evolution (e.g. plant pathogens)  and phylogenetics.

- van Dijk, Bram
Eukaryotes and prokaryotes have distinct genome architectures, with marked differences in genome size, the ratio of coding/non-coding DNA, and the abundance of transposable elements (TEs). As TEs replicate independently of their hosts, the proliferation of TEs is thought to have driven genome expansion in eukaryotes. However, prokaryotes also have TEs in intergenic spaces, so why do prokaryotes have small, streamlined genomes? Using an in silico model describing the genomes of single-celled asexual organisms that co-evolve with TEs, we show that TEs acquired from the environment by horizontal gene transfer can drive the evolution of genome streamlining. The process depends on local interactions and is underpinned by rock-paper-scissor dynamics in which populations of cells with streamlined genomes beat TEs, which beat non-streamlined genomes, in continuous and repeating cycles. Streamlining is maladaptive to individual cells, but delivers lineage-level benefits. Streamlining does not evolve in sexually reproducing populations because recombination partially frees TEs from the deleterious effects they cause.Competing Interest StatementThe authors have declared no competing interest.
- Park, Hye Jin
Compared to their eukaryotic counterparts, bacterial genomes are small and contain extremely tightly packed genes. Therefore, discovering a large number of short repetitive sequences in the genomes of Pseudomonads and Enterobacteria is unexpected. These sequences can independently replicate in the host genome and form populations that persist for millions of years. Here we model the interactions of intragenomic sequence populations with the bacterial host. In a simple model, sequence populations either expand until they drive the host to extinction or the sequence population gets purged from the genome. Including horizontal gene transfer does not change the qualitative outcome of the model and leads to the extinction of the sequence population. However, a sequence population can be stably maintained, if each sequence provides a benefit that decreases with increasing sequence population size. But concurrently, the replication of the sequence population needs to be costly to the host. Surprisingly, in regimes where horizontal gene transfer plays a role, the benefit conferred by the sequence population does not have to exceed the damage it causes. Together, our analyses provide a plausible scenario for the persistence of sequence populations in bacterial genomes. More importantly, we hypothesize a limited biologically relevant parameter range, which can be tested in future experiments.
- Zeng, Quan
Bacterial etiolation and decline (BED), caused by Acidovorax avenae, is an emerging disease of creeping bentgrass on golf courses in the United States. We performed the first comprehensive analysis of A. avenae on a nationwide collection of turfgrass- and maize-pathogenic A. avenae. Surprisingly, our results reveal that the turfgrass-pathogenic A. avenae in North America are not only highly divergent but also belong to two distinct phylogroups. Both phylogroups specifically infect turfgrass but are more closely related to maize pathogens than to each other. This suggests that, although the disease is only recently reported, it has likely been infecting turfgrass for a long time. To identify a genetic basis for the host specificity, we searched for genes closely related among turfgrass strains but distantly related to their homologs from maize strains. We found a cluster of 11 such genes generated by three ancient recombination events within the type III secretion system (T3SS) pathogenicity island. Ever since the recombination, the cluster has been conserved by strong purifying selection, hinting at its selective importance. Together our analyses suggest that BED is an ancient disease that may owe its host specificity to a highly conserved cluster of 11 T3SS genes. © 2017 The American Phytopathological Society.
- Bertels, Frederic
Mobile genetic elements can be found in almost all genomes. Possibly the most common nonautonomous mobile genetic elements in bacteria are repetitive extragenic palindromic doublets forming hairpins (REPINs) that can occur hundreds of times within a genome. The sum of all REPINs in a genome can be viewed as an evolving population because REPINs replicate and mutate. In contrast to most other biological populations, we know the exact composition of the REPIN population and the sequence of each member of the population. Here, we model the evolution of REPINs as quasispecies. We fit our quasispecies model to 10 different REPIN populations from 10 different bacterial strains and estimate effective duplication rates. Our estimated duplication rates range from ~5 3 1029 to 15 3 1029 duplications per bacterial generation per REPIN. The small range and the low level of the REPIN duplication rates suggest a universal trade-off between the survival of the REPIN population and the reduction of the mutational load for the host genome. The REPIN populations we investigated also possess features typical of other natural populations. One population shows hallmarks of a population that is going extinct, another population seems to be growing in size, and we also see an example of competition between two REPIN populations. © 2017 by the Genetics Society of America.
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