Regulation of DNA repair pathway choice
Our DNA constantly faces damage that must be properly repaired to avoid genomic instability and mutations that can trigger cancerous transformation. Breakage of both strands of DNA is the most toxic type of lesion and can be repaired by different repair machineries. How these different pathways are intrinsically regulated to best repair DSBs remains elusive. Our lab builds innovative reporter tools to study the regulation of DSB repair pathway selection in different contexts, including cellular aging.
Dissection of Double Strand Break repair pathways
Because cancer treatments often induce DNA damage or target DNA repair pathways, while patients carrying mutations in DNA repair proteins have a high predisposition to cancers, identification of such factors is critical for both cancer susceptibility diagnosis and development of novel targeted or synergistic therapies. We are using genome-wide and combinatorial Crispr-Cas9 screens to identify novel DNA repair regulators and study their molecular function.
Function of heterochromatin at telomeres.
Telomeres protect the ends of chromosomes from extensive resection and from being recognized as double strand breaks. They are constituted of repetitive DNA sequences tightly packed into heterochromatin and bound by protective proteins. Our lab is dissecting the function of heterochromatin, more specifically histone modifications, in telomere function and maintenance.