Title: The Fenton Reaction in Cells: From DNA ‘Damage’ to Gene Induction
Abstract:
Oxidative and nitrosative stress in cells result in DNA damage due to formation of reactive oxygen and nitrogen species (ROS and RNS). These free radicals, principally carbonate radical and NO plus NO2, react selectively at G and C nucleobases, respectively. We will show that, contrary to popular belief, hydroxyl radical plays no role in endogenous oxidative stress due to the redirection of the Fenton reaction of labile iron to react with cellular bicarbonate. As a consequence, mammalian genomes can directly respond to oxidative stress because G-rich sequences in gene promoters are the common sites of oxidation in the genome. In this case, the DNA repair process leads to non-canonical structures, e.g. G-quadruplexes, that turn on (or off) gene expression. The role of AP endonuclease, a component of the base excision repair pathway, will be discussed.
Bio: See this link.
Keywords: DNA, RNA, oxidative stress, G-quadruplexes, RNA modifications, sequencing, DNA repair, physical organic chemistry, redox iron chemistry
Host: Prof. Bob McMahon