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As part of an active scientific community that studies the DNA damage response (DDR) and its impact on cancer and aging, research in the lab of Matthias Altmeyer is aimed at elucidating cellular mechanisms of genome integrity maintenance and their deregulation in human disease. Here you can explore who we are and what we do. Welcome!

RPA shields inherited DNA lesions for post-MiDAS

Michaela & Aleksandra successfully defend their theses

Two theses presentations, one for a M.Sc. and one for a Ph.D., given as webinars by Michaela and Aleksandra, respectively, mark the successful ending of their research in our lab. Well done and all the best for the steps ahead!

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RPA shields inherited DNA lesions for post-MiDAS

RPA shields inherited DNA lesions for post-MiDAS

In a recent publication we identified replication stress-induced ssDNA lesions in G1 cells. They are found at telomeres in ALT-positive cancer cells and show signs of post-mitotic DNA synthesis (post-MiDAS).

Publications

Postdoctoral Candidates and MSc/PhD Students

Postdoctoral Candidates and MSc/PhD Students

Motivated applications from postdoctoral researchers with a strong interest in genome stability or chromatin biology and willing to apply for fellowships are always encouraged. PhD students are recruited through the Life Science Zurich Graduate School.

Current Openings

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Aleksandra’s paper is out in Nature Communications

June 2021

RPA shields inherited DNA lesions for post-mitotic DNA synthesis

Fragile genomic regions undergo mitotic DNA synthesis (MiDAS). Aleksandra found evidence for post-mitotic DNA synthesis (post-MiDAS). Post-MiDAS occurs at telomeres, particularly in ALT-positive cancer cells, and is amplified by replication stress. Published in Nature Communications.

Further reading:

Lezaja et al., Nat Commun. 2021 Jun 22;12(1):3827.


Magda’s and Stefania’s collaborative paper is out

November 2020

CHD7 and 53BP1 regulate distinct pathways for the re-ligation of DNA double-strand breaks

From a close collaboration with the lab of Haico van Attikum, and with great help from the labs of Sébastien Huet, Alfred Vertegaal, Jessica Downs and Martijn Luijsterburg, the chromatin remodeler CHD7 emerged as an early responder to DNA damage to regulate chromatin dynamics around DNA break sites and initiate repair. Finally out in Nature Communications.

Further reading:

Rother, Pellegrino et al., Nat Commun. 2020 Nov 13;11(1):5775.


Marco’s paper on TRIP12-regulated PARP inhibitor efficiency is out

August 2020

The ubiquitin ligase TRIP12 limits PARP1 trapping and constrains PARP inhibitor efficiency

We found that the ubiquitin E3 ligase TRIP12, through its PAR-binding WWE domain, targets PARP1 for proteasomal degradation, affecting PARP functions and PARP inhibitor efficiency. Congratulations to Marco and big thanks to our collaborators Qingyao Huang and Michael Baudis for their help. Published in Cell Reports.

Further reading:

Gatti et al., Cell Rep. 2020 Aug 4;32(5):107985.


Matteo’s and Federico’s collaborative paper is out

July 2019

Sequential role of RAD51 paralog complexes in replication fork remodeling and restart

Spearheaded by Matteo Berti from Massimo Lopes’ group and Federico Teloni from our lab, our collaborative study on RAD51 and replication fork reversal is finally out in Nature Communications.

Further reading:

Berti, Teloni et al., Nat Commun. 2020 Jul 15;11(1):3531.


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