🚨 Publication Alert 🚨
New review from our #CRC1678 member @riemerlab.bsky.social explores how redox conditions and ROS dynamics shape mitochondrial protein import mapping the redox‑dependent mechanisms linking metabolism, stress, and organelle homeostasis. 🥳
👉 doi.org/10.1002/pro....
Big week at #CRC1678 🚀
Three of our fantastic doctoral researchers interviewed several of our project leaders on key topics around equity and diversity 🎤💬. Final interviews are coming soon, both here and on our website.
Stay tuned and enjoy a behind‑the‑scenes look from our production day 🎥📸
🎓Reflecting on a wonderful graduate symposium: we shared some great moments with inspiring talks and opportunities to connect within our CGA community and beyond. Congrats to all our incredible students from the CGA class of 2022, and big thanks to the class of 2023 for organizing everything. 🎉🍾
CRC1678
🚨 Publication Alert 🚨
New work from our #CRC1678 labs led by @spanier55.bsky.social & @epistrucstab.bsky.social in @embojournal.org shows SLX4IP restrains Bloom syndrome helicase (BLM) to protect replication fork integrity. Congrats to everyone involved🥳
👉 doi.org/10.1038/s443...
Video
🎉 Congrats to Dr. David Meyer @meyerdh.bsky.social from the Schumacher Lab! Our #CRC1678 researcher has been awarded the Klaus Liebrecht-Prize of the @unicologne.bsky.social for his outstanding work on biological aging clocks 👵⏰👴. A fantastic achievement!
👉 uni.koeln/48RZE
CRC1678
🏆 Congratulations to our CGA alumni members Aishwarya Acharya @aishacharya.bsky.social and David Meyer @meyerdh.bsky.social on receiving the Klaus Liebrecht Award 2026 from the University of Cologne for their outstanding doctoral theses! 🎉 We are proud to celebrate this well-deserved success! 👏🧬
📣 News! Deadline Extended! 📣 📅 New Deadline: June 15th, 2026
Good news for those who missed out our last call: The deadline for abstract submissions for the AHA- and EFAR-conferences in October has been extended. Take advantage of this extra time to submit your abstract. uni.koeln/7AYK6
🌈 Heute ist Deutscher Diversity-Tag
Wie gelingt Dialog in polarisierten Zeiten? Darüber sprechen wir am heute bei der Veranstaltung:
„Im Gespräch bleiben: Wissenschaftskommunikation in polarisierten Debatten“
→ Philosophikum, Universität zu Köln
→ 16:00–18:00 Uhr
🔗 uni.koeln/JZQPK
CRC1678
Cologne Graduate School of Ageing Research
Our preprint on how variant U1 snRNAs control transcriptional and splicing homeostasis of hiPSCs is now officially out in @natcomms.nature.com and accessible via this link:
www.nature.com/articles/s41...
This has been the culmination of our work as part of the SPP1935 program funded by @dfg.de
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CRC1678
Cologne Graduate School of Ageing Research
👉Paper alert👈
The @riemerlab.bsky.social discovered that cytosolic PRDX1 acts as an extramitochondrial sink to set mitochondrial H2O2 levels and enable resilience to chronic mitochondrial oxidative stress. Congrats to all researchers involved! 👏
www.sciencedirect.com/science/arti...
Stem cell identity and differentiation require precise gene regulation, yet key regulatory components remain poorly understood. Here, the authors show that variant U1 snRNAs have distinct and essentia...
In our latest preprinted work, Yajie and Kostas combine computational analysis with precision KO of single variant U1 snRNA genes in human iPSCs to find pronounced deregulation of both gene expression and splicing that seem to affect the cell cycle and the differentiation potency of stem cells. 1/n
CRC1218
Faithful DNA replication is essential for genome stability, yet replication forks face constant stress. The Bloom syndrome helicase (BLM) safeguards fork integrity, but excessive BLM activity can itself induce replication stress. We identify SLX4IP as a genome-wide regulator that restrains BLM to maintain replication fork stability. SLX4IP localizes broadly across chromatin with recruitment enhanced under replication stress. Loss of SLX4IP slows replication forks, remodels the replisome, and generates post-replicative single-stranded DNA gaps that are accompanied by elevated nuclear ADP ribose, reflecting compromised replication integrity. These defects are driven by dysregulated BLM activity, establishing SLX4IP as a negative regulator of BLM-dependent replication stress. At ALT telomeres, SLX4IP deficiency triggers ATR signaling, telomere fragility, and accumulation of ALT-associated PML bodies. Here, SLX4IP functions in parallel with FANCM to restrain BLM at ALT telomeres, with co-depletion of SLX4IP and FANCM causing synthetic lethality in ALT-positive cells, a phenotype fully rescued by BLM loss. Together, our results define SLX4IP as a critical genome-wide regulator of replication fork integrity and reveal SLX4IP as a potential vulnerability in ALT-positive cancers.doi.org
Mitochondrial protein import is essential for organelle biogenesis and cellular homeostasis. It operates in an environment that is intrinsically shaped by redox chemistry. Mitochondria are major sour...
Hydrogen peroxide (H2O2) plays a dual role as both a signalling molecule and a mediator of oxidative stress. Although mitochondria are major producers…
