The Project group INF develops the appropriate infrastructure for data handling storage and documentation for the considerable amount of data collected at the CRC1430. It offers numerous opportunities to work at the interface of biomedical research, information sciences, and computer science. Another focus lies on the management of microscopy data, which is established at the Imaging Center Campus Essen (ICCE).

Become part of the Faculty of Biology and Center of Medical Biotechnology at the Campus Essen and apply for the position until the 13th of June 2024!

During cell division the genetic blueprint of an organism is distributed equally between two daughter cells. Eukaryotic cells have evolved a powerful control mechanism which ensures that cell division only proceeds when chromosomes have achieved error-free attachments to the mitotic spindle. In the latest volume of Current Biology, a paper from Stefan Westermann (A1) and his group in collaboration with Andrea Musacchio (A2), Markus Kaiser (B1), and Farnusch Kaschani (Z3) was released. The study sheds light on the long lasting question how cells coordinate the metaphase-anaphase transition with correct spindle attachments. Pleuger et al. define a binding interface of the regulatory kinase Mps1 at the kinetochore, anchor for spindle attachments at the chromosomes as well as signaling hub for mitotic progression. They proceed by showing that the maturation of correct end-on attachments results in the displacement of Mps1 from kinetochores and identify the molecular features of the outer kinetochore leading to the regulation.

The CRC 1430 organized another get-together giving the female members of the CRC1430 a chance to exchange their experiences in scientific research and engage in discussions on how to support the carreers of women. These meetings take place alternatley in the UKE "casino" and at campus Essen at "Brücke" every 6 weeks, giving female scientists the chance to network and discuss various topics.

Join us for our next get-together at “Brücke” June 19th!

The latest paper by Pinki Gahlot from the Meyer lab (A03), published in Molecular Cell, reveals how human cells detect and respond to lipid bilayer disruptions in compromised lysosomes, leading to lysophagy via ubiquitin-triggered pathways instead of membrane repair. SPG20, binding to the repair factor IST1, detects damage-associated lipid-packing defects before membrane rupture. These extensive defects lead SPG20 to recruit and activate ITCH, initiating lysophagy to eliminate the damaged lysosome. These findings underscore the importance of coordinated lysosomal damage responses for maintaining cellular homeostasis.

Read more on the newly decoded signaling pathway for the decomposition of damaged lysosomes here.

Congratulations to Kristina Mrug, who successfully defended her PhD thesis "Regulation of the pulsatory contraction signal network dynamics during cell division" on March 14, 2024.