Wednesday, 28th October, 2015, 12:00

Nucleotide excision repair is impaired by binding of transcription factors to DNA

Somatic mutations are one of the major genetic alterations that contribute to the transformation of normal cell into cancer cell. The rate of somatic mutations appear in great variability across the genome due to chromatin organization, DNA accessibility and replication timing. However, other variables that may influence the mutation rate locally, such as DNA-binding proteins, are unknown. Here we demonstrate that the rate of somatic mutations in melanoma tumors is highly increased at active transcription factor binding sites and nucleosome embedded DNA compared to their flanking regions due to impaired nucleotide excision repair activity.

Speaker: SABARINATHAN RADHAKRISHNAN Biomedical Genomics, GRIB (IMIM-UPF)

Room Aula room (4th floor)