Dissecting the mechanism of DNA lesion repair
Genomic lesions known as interstrand DNA crosslinks (ICLs) form by covalent linkage between the two opposite strands of DNA. ICLs are highly toxic as they can interfere with DNA replication and transcription and can lead to conditions like Fanconi anaemia if left unrepaired. Funded by the EU, the ICL CHROM project aims to delineate the process of ICL repair and identify the key proteins involved, including nucleosome remodelling proteins and histone chaperones. Through novel techniques, scientists will unveil the regulatory mechanism of ICL repair and how cells remodel their chromatin to address ICLs.