NCBR seminar: Catherine Freudenreich

Abstract:

All cells encounter replication barriers upon genome duplication and must overcome those barriers to survive. Many repeat sequences can form alternative DNA structures that interfere with replication and repair. This can lead to disease-causing repeat expansions. Alternatively, breaks within structure-forming repeats cause chromosome deletions and rearrangements, which are common in cancer cells undergoing replication stress. One strategy that cells use to overcome some types of replication barriers or difficult-to-repair lesions is repositioning to the nuclear periphery. I will describe research from my lab on how structure-forming DNA repeats are replicated and repaired and the role of relocation to the nuclear pore in these processes. Recent results on the mechanisms used to move damaged chromosomes to the nuclear pore and the role of this pathway in protecting genome instability will be covered.