Jean Gautier

Many, if not all cancers have unstable genomes. Genomic instability often arises from defects in DNA repair that can drive cancer development; yet the inability of cancer cells to faithfully repair DNA makes them vulnerable to DNA damaging cancer therapies, which are commonly used as first line treatments. The 3D architecture of the genome during DNA repair influences the balance between proper repair, a tumor suppressor mechanism, and pathological repair, that can cause oncogenic chromosome rearrangements. Defining the spatial organization of the genome during DNA repair following DNA damage will help develop a better understanding of cancer etiology and therapy mechanisms. The overarching research goal of the Gautier lab is to define how, within their various chromatin contexts, and at specific cell cycle phases, DNA lesions (e.g. DNA double strand breaks and DNA interstrand crosslinks) and their repair, create genetic mutations and chromosome rearrangements. To achieve this goal, the lab uses diverse experimental approaches, encompassing biochemistry, proteomics, live-cell imaging, super-resolution microscopy, Hi-C and genome-wide rearrangement sequencing. Experimental systems include cell-free extracts that are used as a simple model system to study processes that govern genome stability, including DNA replication control, DNA repair, and the cellular response to DNA damage, as well as cultured normal and tumor cells that are used to model and analyze biological responses to DNA damage.