Circulating to all..Please register and attend! One of the best platforms to meet all mutagenesis enthusiasts!

We;re hiring Junior Group Leaders! 🔬✨
We’re looking for researchers in immunology, chemical biology, AI in biology, or protein design to launch their own independent groups in our collaborative, international environment.

www.nki.nl/news-events/...

This meeting comes highly recommended! Register soon!

A breakage–replication/fusion process explains complex rearrangements and segmental DNA amplification - Nature Genetics This paper introduces breakage–replication/fusion, a genomic rearrangement process underpinning three patterns of copy-number gains found in cancer and other diseases.

www.nature.com/articles/s41...

Rescuing the bacterial replisome at a nick requires recombinational repair and helicase reloading - Nature Communications DNA damage can lead to cell death. Here, the authors show that a simple cut on either strand of DNA can inactivate bacterial chromosome replication. Surprisingly, only a core set of recombination prot...

A cool genetic system to study site-pecific replication fork collapse and repair from the brilliant @winterhalterlab.bsky.social

www.nature.com/articles/s41...

make sure to check out this great meeting 👇

Engineered chromatin readers track damaged chromatin dynamics in live cells and animals - Nature Communications DNA damage threatens genome stability, but its dynamics in living systems remain difficult to track. Here, the authors engineer MCPH1-based protein probes that specifically recognize γH2AX, enabling r...

Check out this beautiful paper by @richardcsilva.bsky.social et al., out now in @natcomms.nature.com. Great new DSB sensors to track DNA break formation and repair in real-time
www.nature.com/articles/s41...

Registration is open!🧬

Join us at Egmond aan Zee (April 19–24, 2026) for the next DNA Repair Meeting. We have an amazing line-up of speakers.

📅 Deadline for early registration: Jan 10, 2026
🔗 dnarepairmeeting-egmond2026.com

Proteome-wide in silico screening for human protein-protein interactions Protein-protein interactions (PPIs) drive virtually all biological processes, yet most PPIs have not been identified and even more remain structurally unresolved. We developed a two-step computational...

Thrilled to share that the final piece of my PhD work is now on bioRxiv! biorxiv.org/content/10.1... With support from @nvidia and the @NSF, we used AlphaFold to screen 1.6M+ protein pairs, revealing thousands of potential novel PPIs. All data can be viewed at predictomes.org/hp

Congrats Arnab and team!!

Congrats!!

We are excited to welcome Evi Soutoglou and @rubenvanboxtel.bsky.social as our guest speakers at the upcoming GIIN webinar on Tuesday, November 4th at 5 PM Rome / 11 AM NYC.
Join us on zoom: uniroma1.zoom.us/j/95149984403
Register here to become part of our community: docs.google.com/forms/d/e/1F...

Congrats, beautiful work!

PhD student DNA repair in kidney cancer | Werken bij UMC Groningen

We have an open position for a PhD student to join our team. If you have an interest in cancer biology, genome maintenance, or both, please apply! Details can be found in the link below. With @marcelvanvugt.bsky.social.

werkenbijumcg.nl/-/vacatures/...

Congrats Martijn, well deserved!

Congrats, very exciting work!

The Genome Integrity Webinar Series continues on Tuesday, May 6th at 5PM (Rome) / 11AM (New York) with an exciting discussion on DNA damage response and repair @kajastelab.bsky.social
Join via Zoom: uniroma1.zoom.us/j/95149984403

Mutational signature catalogue (MUSIC) of DNA double-strand break repair Genome alterations arise from inaccurate DNA repair, accumulating into distinct mutational signatures. Here, we investigate the role of every genomically encoded gene in double-strand break (DSB) repa...

Very exciting work by the Tijsterman lab www.biorxiv.org/content/10.1...

A must for all DNA repair aficionados!

Egmond DNA Repair Meeting → April 19–24, 2026 🇳🇱
✔️ Confirmed top speakers
✔️ Ample opportunities for talks & posters

Don’t miss it: dnarepairmeeting-egmond2026.com

@puckknipscheer.bsky.social, @luijsterburglab.bsky.social, @marcelvanvugt.bsky.social, @sylvie-noordermeer.bsky.social, @titiasixma.bsky.social, @marcelvanvugt.bsky.social, @marteijnlab.bsky.social

CIP2A is required for mitotic recruitment of the SLX1/XPF/MUS81 tri-nuclease complex to replication stress-induced DNA lesions to maintain genome integrity Perturbed DNA replication can lead to incompletely replicated DNA when cells enter mitosis and can interfere with chromosome segregation. Cells therefore require mechanisms to resolve these lesions du...

Extremely happy to share that my main PhD project about CIP2A-TOPBP1 and the SMX complex is now available online as pre-print.

Huge thanks to all co-authors but especially @marcelvanvugt.bsky.social for giving me the opportunity to work on this exciting project!

www.biorxiv.org/content/10.1...

REV7 functions with REV3 as a checkpoint protein delaying mitotic entry until DNA replication is completed How cells ensure that they enter mitosis after completing replication of their genome is not fully resolved. Sobkowiak et al. describe a checkpoint involving REV7. This checkpoint has mechanistic similarities to the spindle anaphase checkpoint mediated by…

REV7 functions with REV3 as a checkpoint protein delaying mitotic entry until DNA replication is completed

A CPC-shelterin-BTR axis regulates mitotic telomere deprotection - Nature Communications Here the authors reveal how telomeres signal mitotic stress. A key protein network alters their structure exposing telomere ends to signal mitotic stress, ultimately triggering a controlled DNA damage...

1/Out today in @naturecomms.bsky.social,

“A CPC-shelterin-BTR axis regulates mitotic telomere deprotection”.

Here we identify the mechanism that unwinds telomere-loops (t-loops) during mitotic arrest to activate the DNA damage response and signal mitotic stress.

www.nature.com/articles/s41....

WEE1 inhibitors synergise with mRNA translation defects via activation of the kinase GCN2 Inhibitors of the protein kinase WEE1 have emerged as promising agents for cancer therapy. In this study, we uncover synergistic interactions between WEE1 small-molecule inhibitors and defects in mRNA translation, mediated by activation of the integrated stress response (ISR) through the kinase GCN2. Using a pooled CRISPRi screen, we identify GSPT1 and ALKBH8 as factors whose depletion confer hypersensitivity to the WEE1 inhibitor, AZD1775. We demonstrate that this synergy depends on ISR activation, which is induced by the off-target activity of WEE1 inhibitors. Furthermore, PROTAC-based WEE1 inhibitors and molecular glues show reduced or no ISR activation, suggesting potential strategies to minimise off-target toxicity. Our findings reveal that certain WEE1 inhibitors elicit dual toxicity via ISR activation and genotoxic stress, with ISR activation being independent of WEE1 itself or cell-cycle status. This dual mechanism highlights opportunities for combination therapies, such as pairing WEE1 inhibitors with agents targeting the mRNA translation machinery. This study also underscores the need for more precise WEE1 targeting strategies to mitigate off-target effects, with implications for optimising the therapeutic potential of WEE1 inhibitors. ### Competing Interest Statement The authors have declared no competing interest.

in parallel, a study that describes very similar results was posted by the lab of Stephen Jackson from Cambridge UK:
www.biorxiv.org/content/10.1...

Thanks to the many collaborators; the labs of Thijn Brummelkamp, Alexander van Oudenaarden, Steven de Jong, Frank Sicheri, Marvin Tanenbaum @marvintanenbaum.bsky.social @jervdberg.bsky.social @rinskjetjeerdsma.bsky.social @mauritsroorda.bsky.social @daaninthelab.bsky.social

WEE1 inhibitors trigger GCN2-mediated activation of the integrated stress response The WEE1 kinase negatively regulates CDK1/2 to control DNA replication and mitotic entry. Genetic factors that determine sensitivity to WEE1 inhibitors (WEE1i) are largely unknown. A genome-wide inser...

Happy to post a new study on BioRxiv, where we show Integrated Stress Response activation as an off-target effect of multiple clinically evaluated WEE1 inhibitors. Team effort with the lab of Dan Durocher @durocher1.bsky.social and many others. www.biorxiv.org/content/10.1...

Congrats Agnel, very exciting work!

Very nice work! Congrats

The transcriptomic architecture of common cancers reflects synthetic lethal interactions - Nature Genetics Tumor cells upregulate compensatory buffering genes following tumor suppressor loss. These genes may represent new synthetic lethal partners that could be harnessed therapeutically.

We show transcriptomic buffering of tumour suppressor loss via syn. lethal genes is not anecdotal but a cancer hallmark. Buffering also seen in BRCAness, predicts penetrant syn leth effects and outcome. @icr.ac.uk @cancerresearchuk.org @breastcancernow.bsky.social www.nature.com/articles/s41...

SAVE THE DATE! The next EMBO | EMBL Symposium on 'DNA replication and genome maintenance: from basic biology to disease' will be held October 20-23, 2026.
 
Organized by Helle Ulrich (IMB), Johannes Walter (Harvard) and Anja Groth (Danish Cancer Institute).

www.embl.org/about/info/c...