Jan Padeken
The interplay between heterochromatin, the stress response & premature ageing
The separation of our genome into euchromatin and heterochromatin is essential for faithfully orchestrating gene expression programmes and maintaining cellular resilience. Across a wide range of species, ageing is correlated with a reduction and reorganisation of heterochromatin. In healthy, young cells, heterochromatin marked by histone H3 lysine 9 methylation (H3K9me) represses repetitive elements and lineage-specific genes. Loss of H3K9me causes genome instability, loss of tissue integrity and premature ageing. Using C. elegans, we combine genetics, genomics and quantitative microscopy to study the impact of genotoxic stresses on the establishment and maintenance of heterochromatin, with the goal of better understanding the complex interplay between stresses experienced throughout life, the epigenome and ageing.
Research website
Positions held
- 2022: Group Leader, Institute of Molecular Biology (IMB), Mainz
- 2013 - 2022: Postdoctoral researcher, Friedrich Miescher Institute, Basel
Education
- 2013: PhD in Cell Biology, Max Planck Institute of Immunobiology and Epigenetics
- 2009: Diploma in Biology, Albert-Ludwigs University, Freiburg
- 2006: Vordiploma in Biology, RWTH Aachen University
Selected publications by Jan Padeken
Delaney CE, Methot SP, Kalck V, Seebacher J, Hess D, Gasser SM and Padeken J (2022) SETDB1-like MET-2 promotes transcriptional silencing and development independently of its H3K9me-associated catalytic activity. Nat Struct Mol Biol, 29:85–96 Link
Padeken J, Methot SP and Gasser SM (2022) Establishment of H3K9-methylated heterochromatin and its functions in tissue differentiation and maintenance. Nat Rev Mol Cell Biol, doi: 10.1038/s41580-022-00483-w Link
Methot SP*, Padeken J*, Brancati G, Zeller P, Delaney CE, Gaidatzis D, Kohler H, van Oudenaarden A, Großhans H and Gasser SM (2021) H3K9me selectively blocks transcription factor activity and ensures differentiated tissue integrity. Nat Cell Biol, 23:1163–1175 (*indicates joint contribution) Link
Padeken J, Methot S, Zeller P, Delaney CE, Kalck V and Gasser SM (2021) Argonaute NRDE-3 and MBT domain protein LIN-61 redundantly recruit an H3K9me3 HMT to prevent embryonic lethality and transposon expression. Genes Dev, 35:82–101 Link
Delaney CE*, Methot SP*, Guidi M*, Katic I, Gasser SM and Padeken J (2019) Heterochromatic foci and transcriptional repression by an unstructured MET-2/SETDB1 co-factor LIN-65. J Cell Biol, 218:820–838 (*indicates joint contribution) Link