RAD16 & RAD7 Gene Knockout: Investigating The Role of Genes on UV-Induced DNA Damage Repair in Yeast
Posted on Wednesday, April 9th, 2025
Skin cancer is the most prevalent cancer in Canada, accounting for nearly one-third of new diagnoses annually. Ultraviolet (UV) radiation is a major contributor which induces DNA lesions that, if left unrepaired, lead to oncogenic mutations. The Nucleotide Excision Repair (NER) pathway is essential for repairing UV-induced lesions, yet the roles of specific genes within this pathway remain unclear. This study investigates RAD7 and RAD16, two key NER genes, in UV damage repair using Saccharomyces cerevisiae. Knockout mutants were generated via homologous recombination and validated by PCR. Repair efficiency was assessed through survival assay. RAD7 and RAD16 knockouts exhibited reduced repair efficiency compared to wild-type strains. These findings aim to clarify their roles in lesion recognition and repair. Additionally, this research could provide insights relevant to skin cancer prevention and therapeutic strategies, with broader implications for genetic disorders involving defective DNA repair.