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Peter Andersen

Laboratory on Genetic Innovation


Despite its often harmonic appearance, all life forms exist in a constant evolutionary arms race. This arms race is caused by pervasive evolutionary and genetic conflicts. Such conflicts take place between species of prey, predators, parasites and their hosts. But conflicts are also present within species where selfish genetic elements such as transposons have often opposing evolutionary ‘interests’ to the host genome. An arms race is a state of rapid innovation and in biology innovation takes place by changes in the function of genes or by the emergence of entirely new genes. Evolutionary arms races are therefore rich sources of genetic innovation.

We study the genetic innovation resulting from genetic conflicts within animal genomes to uncover:

  • New concepts in gene regulation and germline biology
  • The molecular mechanisms underlying arms race evolution of intragenomic conflicts

Latest news

Publication in Cell: Smuggling route for cells protects DNA from parasites

Our cells have safety mechanisms that keep genetic parasites - such as viruses and transposons - in check while important genes of the host cell can remain active. Together with colleagues in Julius Brennecke's group at the Vienna BioCenter, Peter has now found the answer to one of the big open questions in understanding how the defence mechanisms against transposons work.

Peter Refsing Andersen appointed member of the Young Academy (DUA)

DUA (“Det Unge Akademi”) is a scientific academy for young talented researchers in Denmark under the auspices of the Royal Danish Society of Sciences and Letters. There are 40 members of DUA in total.

Peter Refsing Andersen awarded the Hallas-Møller Emerging Investigator grant

Peter Refsing Andersen has been awarded a Hallas-Møller Emerging Investigator grant of DKK 10 mio. (ca. Euro 1,342,320) over the next five years to establish a research group at the Department of Molecular Biology and Genetics, AU, to study genetic innovation in the arms race between selfish genes and host genomes.