The main objective of our lab is to study mechanisms that promote genome duplication in human cells. Our project focuses on understanding how chromatin remodelers act at replication forks to promote DNA synthesis. Forks undergo multiple processing events when exposed to replication stress.
These events give rise to replication intermediates that can convert to toxic breaks if left unrepaired. Recent studies demonstrate that the presence of single-strand DNA gaps in nascent DNA can cause genome instability and is a determinant of chemo sensitivity. Our work addresses the role of a conserved nucleosome remodeler, SNF2L, in DNA synthesis.
SNF2L travels with replication forks, but the mechanism of action is poorly characterized. Using the comet assay protocol allows us to assess consequences in fork stability when SNF2L is absent.
