UC Davis researchers have found a new pathway for repairing DNA damaged by oxygen radicals. The results are published this week in the journal Proceedings of the National Academy of Sciences.
"This new inducible pathway gives cells greater capacity to repair oxidative damage," said Peter Beal, professor of chemistry at UC Davis and senior author of the paper.
As part of its inflammatory response, the body's immune system produces oxygen radicals, or reactive oxygen species, to kill bacteria, parasites or tumors. But chronic inflammation, for example in the gut, has been linked to cancer, said co-author Professor Sheila David, also of the Department of Chemistry.
Oxygen radicals are strongly linked to cancer and aging and are also formed during metabolism and upon exposure to environmental toxins and radiation. Understanding more about how this damage can be repaired could lead to a better understanding of the causes of some cancers.
Oxygen radicals can react with the four bases that make up the "letters" of DNA -- A, C, G and T -- so that the "spelling" of genes gets changed. The accumulation of spelling errors (called mutations) can lead to cancer.
David's laboratory studies an enzyme called NEIL1 that detects and repairs these aberrant or damaged bases before changes in the genome become permanent.
Beal's group works on RNA editing. The first step in turning a gene into a protein is to make a copy of the DNA in RNA. This messenger RNA is then translated into the chain of amino acids that makes up a protein. In some cases, this RNA is "edited" between the transcription from DNA and the translation into protein.
At a conference last year, Beal -- who happens to be David's husband -- spotted NEIL1 among a list of genes that had just been discovered to be subject to RNA editing, and passed the news on to David.
On investigation, they found that NEIL1's messenger RNA is edited by an enz
|Contact: Andy Fell|
University of California - Davis