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. CYREN is a small protein that interacts with the Ku heterodimer and inhibits NHEJ during the S and G2 phases of the cell cycle, thereby promoting Homologous Recombination. Our lab focuses on the exact mechanism of action and regulation of CYREN.
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 Crispr-Cas9 libraries to screen for novel DNA repair proteins and regulators and to study their molecular function.
Telomeric and cellular roles of TERRA
Telomeres protect the ends of chromosomes from extensive resection and from being recognized as double strand breaks. They are constituted of repetitive DNA sequences, protective proteins and a non-coding RNA called TERRA. Our lab focuses on telomeric and extra-telomeric functions of TERRA.