Max Planck Research Group Panier

Genome Instability and Ageing

Cells are constantly exposed to influences that cause DNA damage, both from inside the cell and from the environment. To counteract this, cells have sophisticated signaling pathways at their disposal that detect such DNA lesions and facilitate their timely repair. We are investigating these cellular DNA damage response pathways to understand how they ensure genome stability and how their dysfunction contributes to human ageing and disease.

The stability of genetic material is of fundamental importance for cellular homeostasis and organism viability. Yet, cells are always exposed to environmental and endogenous genotoxic agents that threaten DNA integrity. To protect their genomic stability, cells mount a complex network of DNA damage response pathways that activate cell cycle checkpoints, coordinate DNA repair, regulate gene expression and, if necessary, induce apoptosis. Indeed, DNA damage signalling and repair is a powerful barrier to tumourigenesis, and defects in these pathways promote cell proliferation and genomic instability in pre-malignant lesions. Critically, genomic instability is also a driver of many aspects of cellular ageing and is linked to the onset of age-associated diseases such as neurodegeneration and cancer.

Our research mission is to uncover how DNA damage response (DDR) pathways preserve genome integrity and coordinate with other cellular processes to maintain organismal health. In particular, we aim to understand how the DDR is integrated into broader networks of chromatin organization, transcription, and RNA metabolism. By revealing how these systems interact, we seek to define the principles governing genome stability in normal physiology and identify how their disruption drives aging and disease.

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Selected Publications

SLX4IP limits replication stress globally and at ALT telomeres.
Spindler, J., Pandolfo, F., Koch, A.E., Piccirillo, P., Jordahl, D., Venkatesh, N., Suresh, D., Ylvisaker, K.R., Jopkiewicz, A., Bihler, J., Buschbaum, S., Morgenstern, M., Overmyer, K.A., Vincendeau, E., Cooj, J.J., Wei, P.-W., Hänsel-Hertsch, R., Mehta, K.P.M., Panier., S.
(2026) EMBO Jhttps://doi.org/10.1038/s44318-026-00790-4

SLX4IP Antagonizes Promiscuous BLM Activity during ALT Maintenance
Panier, S., Maric, M., Hewitt, G., Mason-Osann, E., Gali, H., Dai, A., Labadorf, A., Guervilly, J. H., Ruis, P., Segura-Bayona, S., Belan, O., Marzec, P., Gaillard, P. H. L., Flynn, R. L., Boulton, S. J.
(2019) Mol Cell, 76, 1, 27-43 e11

Double-strand break repair: 53BP1 comes into focus
Panier, S., Boulton, S. J.
(2014) Nat Rev Mol Cell Biol, 15, 1, 7-18

Tandem protein interaction modules organize the ubiquitin-dependent response to DNA double-strand breaks
Panier, S., Ichijima, Y., Fradet-Turcotte, A., Leung, C. C., Kaustov, L., Arrowsmith, C. H., Durocher, D.
(2012) Mol Cell, 47, 3, 383-95

The MMS22L-TONSL complex mediates recovery from replication stress and homologous recombination
O'Donnell, L., Panier, S., Wildenhain, J., Tkach, J. M., Al-Hakim, A., Landry, M. C., Escribano-Diaz, C., Szilard, R. K., Young, J. T., Munro, M., Canny, M. D., Kolas, N. K., Zhang, W., Harding, S. M., Ylanko, J., Mendez, M., Mullin, M., Sun, T., Habermann, B., Datti, A., Bristow, R. G., Gingras, A. C., Tyers, M. D., Brown, G. W., Durocher, D.
(2010) Mol Cell, 40, 4, 619-31

The RIDDLE syndrome protein mediates a ubiquitin-dependent signaling cascade at sites of DNA damage
Stewart, G. S., Panier, S., Townsend, K., Al-Hakim, A. K., Kolas, N. K., Miller, E. S., Nakada, S., Ylanko, J., Olivarius, S., Mendez, M., Oldreive, C., Wildenhain, J., Tagliaferro, A., Pelletier, L., Taubenheim, N., Durandy, A., Byrd, P. J., Stankovic, T., Taylor, A. M., Durocher, D.
(2009) Cell, 136, 3, 420-34