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ARS Home » Research » Publications at this Location » Publication #95253
Title: IRON, DNA AND CHROMATIN REMODELING

Author
item Leong, Sally
item YUAN, WALTER - UNIVERSITY OF WISCONSIN
item KEARNEY, L - UNIVERSITY OF WISCONSIN

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 5/1/1998
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Iron present in loosely bound or unchelated forms within cells can act catalytically to produce DNA damaging and lipid peroxidizing oxygen radicals. Living cells regulate the transport and storage of iron to minimize free radical damage. When this regulation is disrupted the consequences on cellular growth and survival are dramatic. Mutations in fur, a gene regulating high affinity iron uptake in E. coli, lead to 8-fol elevated levels of intracellular iron and increased rates of cell death and mutagenesis during aerobic growth. An AFT1up mutation in yeast leads to deregulated iron uptake and reduced cell growth in iron-replete medium. The effects of iron overload are aggravated by mutations in DNA repair systems demonstrating that DNA damage is prevalent under these conditions. In humans, hemachromatosis leads to iron loading in the liver, heart and pancreas, resulting in cirrhosis of the liver, pancreatic fibrosis and cardiac dysfunction, as well as increased risk of hepatocellular carcinoma Despite the wealth of information on the negative impact of iron overload in cells, surprising little is known about the molecular basis or iron- mediated, transcriptional control of iron uptake in eucaryotes where transcription occurs on a chromatin template.