Frontiers in DNA Repair Meeting
Berlin – Brandenburg Academy of Sciences, Germany
September 12, 2016
It was in June when I received an email informing me that I had been selected to give a short talk in the “Frontiers in DNA repair” meeting at the Berlin –Brandenburg academy of sciences. It was a matter of pride for me to present my research in such a revered institute, where many great names have left a mark on the Academy’s history of more than 300 years. This one-day conference was organised by Michela Di Virgilio(MDC Berlin) and comprised of talks by 8 invited speakers from the USA, UK, and Europe as well as 4 short talks selected from the abstracts.
The symposium started with Titia DeLange giving a keynote lecture on how the Shelterin complex protects the telomere from DNA damage and maintains genome stability. She presented some new data from her lab on how POT1 protects the telomere from RPA binding and preventing ATR activation.
Michael Lisby (Copenhagen) gave a spectacular talk on a novel factor identified by SILAC-MS analysis, Mte1 (Mph1- associated telomere maintenance1). Mte1 is a yeast orthologue of ZGRF1 that associates with Mph1 (FANC M family protein) and both colocalize at DNA damage-induced foci and at dysfunctional telomeres.
The second session on genomic integrity was chaired by Ylli Doksani and started with Jiri Lukas’s talk on how a cell deals with endogenous DNA damage and DNA repair signaling mechanism. Lukas lab is focussed on understanding the DNA damage generated during replication. He showed how unresolved replication intermediates can produce DNA breaks leading to genome instability.
Bruno Vaz (Postdoc from Ramadan Lab, Oxford Oncology Department), gave a short talk on a novel metalloprotease SPRTN which removes DNA-protein crosslinks (DPC) during S-phase. SPRTN protease acts a main DPC repair pathway responsible for preventing genomic instability, ageing and cancer.
The final session mainly focussed on harnessing the DNA damage response with talks by Steve Jackson and Thomas Helleday. Steve showed how cells respond to different DNA damage repair pathways, and also focussed on the clinical trials of PARP inhibitor and drugs inhibiting BRCA pathways in breast cancer patients.
Helleday talked about MTH1, a hot cancer drug target. His group founded this drug and is under clinical phase trial1 under the name “MASTIFF, which stands for “Mth1, A phase I,Study on Tumor Inhibition, First in human, First in class clinical trial”
My abstract on “Radiation sensitivity and DNA damage response mechanism in planarian stem cells” was accepted for a short talk in this meeting. I introduced planaria as an emerging model system where we can study DNA damage in the context of adult stem cells. Given the conservation between planarian stem cells and mammalian cells, we can answer how cells repair DNA damage in vivo after ionizing radiation. Using RNAi screen I have shown the role of different DNA repair pathways in stem cell survival post irradiation. The talk was well received by the scientists and I also got the opportunity to interact, and exchange ideas and views during the conference.
This meeting gave me the chance to interact with a number of academics and professionals from different countries who have similar research interests. This has helped me in starting to build lasting networks that will hold me in good steed in my future endeavours. Finally, I would like to thank The Keble Association, Oxford; British Society for Cell Biology (BSCB) and British society for Developmental Biology (BSDB) for awarding travel grants to attend the meeting. This conference was very interesting and enriched my experience with more information, knowledge, and confidence.