TUCSON, Ariz. — A break-through discovery in cellular and molecular medicine. A certain DNA structure is more unstable than researchers first thought.
About half of our genome is made out of retro-viruses, which are DNA elements that can damage our cells. Heterochromatin keeps those retro-viruses at bay, preventing them from damaging our cells.
"We've always cared about heterochromatin because without heterochromatin, we would open ourselves up to all sorts of diseases," said Keith Maggert, a UA associate professor in cellular and molecular medicine.
Maggert has studied heterchromatin for 25 years, and in this stage of his research, he studies with drosophila -- the fruit fly.
The stability of heterochromatin is necessary to keeping our cells safe from the retro-viruses. About five years ago, Maggert and others in the field realized that it's not as stable as they once thought.
"We thought originally that it was pretty stable, and once it was created on these toxic sequences, they were shut down for pretty much all time and we were safe from them. But it turns out, that through the course of a lifetime, heterochromatin weakens," said Maggert.
A lot of complex diseases have heterochromatin defects; the most common being cancer. Heterochromatin is only inactive for a short amount of time, but Maggert said we can't tell what damage has occurred during the time it wasn't functioning.
"Those cells are forever mutated just laying in wait to become pre-cancerous or cancerous," said Maggert.
He said the cellular biology of fruit flies and human are similar. Studying the flies will allow Maggert and his team to examine the first events that happen in the beginning of human cancer.
Maggert is in year three of a five-year $2.5 million Transformative Research Award grant from the National Institutes of Health.
