I have received my PhD in Biology from EMBL with a joint degree from Heidelberg University. During my PhD I worked on understanding the impact of transposable elements on gene regulation by studying LTR elements in developing mouse embryo. In a collaboration with Didier Trono from EPFL Switzerland we identified KAP1/TRIM28 as the master epigenetic regulator of Endogenous Retroviral elements. After a short bridging postdoc period at EMBL I have started my postdoc at Max Planck Institute of Immunobiolgy and Epigenetics in Freiburg. During my postdoc I worked with an abundant nuclear RNA helices, DHX9. We discovered that DHX9 suppresses RNA processing defects which are caused by the large secondary structures of Alu repeats embedded within genes. This work has paved the way to understanding the contribution of RNA binding proteins in enabling the transposable element expansions in genomes. We have as well developed new methods to explore Protein-RNA interactions in order to overcome the difficulties of conventional CLIP technologies. Since December 2018, I am heading the Max Planck Research Group for Quantitative RNA Biology at Max Planck Institute for Molecular Genetics in Berlin.
Education and positions held
- 2018 – present
- Max Planck Research Group Leader at the MPI for Molecular Genetics, Berlin
- 2012 – 2018
- Max Planck Institute of Immunobiology and Epigenetics, Postdoc with Dr. Asifa Akhtar, Department of Chromatin Regulation
- 2011 – 2012
- European Molecular Biology Laboratory (EMBL) Heidelberg, Postdoc with Dr. François Spitz, Developmental Biology Unit
- 2007 – 2011
- European Molecular Biology Laboratory (EMBL) Heidelberg, Ph.D. with Dr. François Spitz, Developmental Biology Unit
- 2003 – 2007
- Middle East Technical University (METU) Ankara, Turkey, B.Sc. Molecular Biology and Genetics”
Understanding how our genome works is one of the most important goals of biological sciences. With only four letters A, T, C and G, the alphabet of our genome is deceptively simple. However, the language built with these four letters is proving to be extremely complex and full of surprises. For example, as the human genome was sequenced at the turn of the century, it became clear that at least half of our genome is composed of so-called selfish genetic elements: transposons and viruses while the protein-coding part of genome makes up less than 2% of our genome. How is this possible, and what does it really mean?
On the one hand, we know that transposons/viruses pose a danger to our genome integrity and cause diseases, on the other hand it is becoming more and more clear that at the same time, paradoxically, they play crucial roles in creating incredible biological complexity. How do our cells perform this balancing act?
In our laboratory we are motivated by these fundamental questions and we will work on several aspects of transposon-host interactions and their impact on the evolution and wiring of post-transcriptional RNA processing networks. We will investigate how strategies that suppress, delay or neutralize transcribed transposons/viruses shape our transcriptomes and through evolution, our genomes.
- Aktas T.; Ilik I.A.; Maticzka D.; Bhardwaj V.; Rodrigues C.P.; Manke T.; Backofen R.; Akhtar A.; DHX9 suppresses RNA processing defects originating from the Alu invasion of human genome, Nature,544 (7648), 115-119, 2017
- Rowe H.M.; Jakobsson J.; Mesnard D.; Rougemont J.; Reynard S.; Aktas T.; Maillard P.V.; Layard-Liesching H.; Verp S.; Marquis J.; Spitz F.; Constam D.B.; Trono D.; KAP1 controls endogenous retroviruses in embryonic stem cells, Nature, 463, 7278, 237-240, 2010
- Ilik, I.A., Aktas, T., Maticzka, D., Backofen, R. and Akhtar, A., 2020. FLASH: ultra-fast protocol to identify RNA–protein interactions in cells. Nucleic acids research, 48(3), pp.e15-e15.
- Rowe H.M.; Friedli M.; Offner S.; Verp S.; Mesnard D.; Marquis J.; Aktas T.; Trono D.; De novo DNA methylation of endogenous retroviruses is shaped by KRAB-ZFPs/KAP1 and ESET, Development, 140, 3, 519-529, 2013
- Basilicata, M.F.†, Bruel, A.L.†, Semplicio, G.*, Valsecchi, C.I.K.*, Aktaş, T.*, Duffourd, Y., Rumpf, T., Morton, J., Bache, I., Szymanski, W.G. and Gilissen, C., 2018. De novo mutations in MSL3 cause an X-linked syndrome marked by impaired histone H4 lysine 16 acetylation. Nature genetics, 50(10), p.1442, 2018
†, * equal contribution