Laboratory Valentin Flury

Chromatin dynamics across the cell cycle

The Flury lab is interested in dissecting the regulatory mechanisms maintaining epigenetic (chromatin) states across the cell cycle using genomic and proteomic approaches with high temporal and spatial resolution. We track these chromatin states over time after intrinsic challenges such as DNA replication, mitosis or DNA damage to reveal the governing principles of chromatin plasticity and stability during homeostasis, differentiation and diseased states.

Multicellular organisms display an impressive variety of different cell types even though they all contain the same genetic information. This difference is in part controlled by their epigenome, or more specifically, by chromatin states that regulate and maintain cell type-specific gene expression programs. Yet, chromatin undergoes dramatic alterations during each cell division, especially during DNA replication, where chromatin is disrupted to allow DNA synthesis. We strive to understand how chromatin states are propagated, restored, and regulated during this process and to what extent their deregulation contributes to changes in cell identity in both healthy and diseased cells.


We aim to achieve the following goals to obtain mechanistic insights into epigenome maintenance and propagation: i) Identify factors involved in epigenome propagation during DNA replication; ii) Dissect common and cell type-specific principles of chromatin restoration and; iii) decipher the impact of signaling cues altering these processes in stem cell homeostasis and during differentiation. Ultimately, our plan includes iv) developing novel tools to track chromatin states to monitor locus-specific chromatin plasticity over time across multiple cell divisions.



We employ both established and novel pulse-chase approaches to define and monitor chromatin composition at the local or global level. We utilize genomics (SCAR/ChOR-seq) and proteomics (iPOND, APEX) in combination with fast-acting genetic perturbations aiming to reveal the multilayered chronology of chromatin plasticity. Our studies use fission yeast (Schizosaccharomyces pombe) and mouse embryonic stem cell cultures to identify both common and unique principles of chromatin state propagation in eukaryotes.



Maintaining chromatin states is essential for preserving cellular identity and is often misregulated in many diseases, particularly in cancer. Yet, the temporal order of events leading to disease remains poorly understood due to a lack of appropriate tools to track chromatin state changes over time. Therefore, to understand the underlying principles of disease formation, we aim to track the spatiotemporal changes across cell divisions. This will enable us to define cell cycle stages that are susceptible to modulate epigenome plasticity and cell identity.


Selected Publications

Flury V, Groth A (2024)
Safeguarding the epigenome through the cell cycle: a multitasking game.
Current Opinion in Genetics & Development 85:102161.
Flury V, Reverón-Gómez N, Alcaraz N, Stewart-Morgan KR, Wenger A, Klose RJ, Groth A (2023)
Recycling of modified H2A-H2B provides short-term memory of chromatin states.
Cell 186 (5),1050-1065.
Wenger A, Biran A, Alcaraz N, Redó-Riveiro A, Sell AC, Krautz R, Flury V, Reverón-Gómez N, Solis-Mezarino V, Völker-Albert M, Imhof A, Andersson R, Brickman JM, Groth A (2023)
Symmetric inheritance of parental histones governs epigenome maintenance and embryonic stem cell identity.
Nature Genetics 55 (9), 1567-1578.
Flury V, Georgescu PR, Iesmantavicius V, Shimada Y, Kuzdere T, Braun S, Bühler M (2017):
The Histone Acetyltransferase Mst2 Protects Active Chromatin from Epigenetic Silencing by Acetylating the Ubiquitin Ligase Brl1.
Molecular Cell 67 (2), 294-307.
Kowalik KM, Shimada Y, Flury V, Stadler MB, Batki J, Bühler M (2015)
The Paf1 complex represses small-RNA-mediated epigenetic gene silencing.
Nature 520 (7546), 248-252.

More publications

Go to Editor View