Our collaboration with the Francis Barr lab has been published in Nature Cell Biology. The findings show how cells can "remember" how long they spent in mitosis - a critical phase in the cell cycle. If the cells spend too long in mitosis, they are able to "memorise" this and then stop proliferating. These findings likely have important implications for tumour suppression as it prevents cells acquiring genome instability - a key cause of cancer - that could be passed on to new cells.
Our collaboration with the Ivan Ahel lab has been published in EMBO Reports. The findings show that nucleic acids can be modified with ubiquitin, adding to the growing list of molecules that ubiquitin can be attached to. Excited to see what this modification does in cells, the enzymes that control it, and whether this can be harnessed for therapeutic use.
We welcome two new starters to the lab: Yutong (DPhil candidate) and Megan (MBiochem Part II)
The lab was again awarded the LEAF Gold award for sustainability:
https://sustainability.admin.ox.ac.uk/leaf-award-winners#collapse4935206
Welcome to two summer students Suki Fogg (University of Oxford) and Mask Federovskyy (Harvard University)
Viva time at the University of Birmingham with Christian Speck and Divyasree Poovathumkadavil from the Gambus lab - congratulation Divya on your thesis and defence.
Congratulations to Matt on successfully passing his viva! Matt initiated our cell biology work on the ZUP1 DUB, establishing microscopy pipelines and performing our first CRISPR-Cas9 screen. He made a huge impact during his time in the lab and will be missed - good luck in your future Matt.
A huge 'thank you' to his examiners: Nick Lakin (University of Oxford) and Jo Morris (University of Birmingham).
Welcome to four new starters: Leslye (postdoctoral researcher), Alex (DPhil candidate), Xianzhen (DPhil candidate), and Madeline (MBiochem Part II).
Our collaboration with the Nick Lakin lab has now been published in Nature Communications. It identifies a poorly characterised protein called C16orf72/HAPSTR1 as being important for cell survival in the absence of PARP1/2 enzymes.