A new discovery from researchers at Huntsman Cancer Institute (HCI) at the University of Utah concerning a fundamental understanding about how DNA works will produce a “180-degree change in focus” for researchers who study how gene packaging regulates gene activity, including genes that cause cancer and other diseases. The discovery, by Bradley R. Cairns, PhD, Senior Director of Basic Science at HCI and a professor in the Department of Oncological Sciences, is reported in this week’s online issue of the journal Nature.
Cairns’s research focuses on chromatin remodeling complexes (CRCs), which are cellular protein complexes that behave like motors, expanding or compacting different portions of DNA to either express or silence genes, respectively. Before, scientists thought that the motor within CRCs waits at rest until it receives instructions. Cairns and co-author Cedric R. Clapier show that the motor within a key CRC responsible for gene packaging and assembly is intrinsically turned on, and instead requires specific instructions to turn it off.
“Many articles in the research literature show that CRCs are mutated in cancer cells. They are intimately involved in regulating gene expression—responsible for correctly packaging genes that control growth proliferation and for unpackaging tumor suppressors,” said Cairns. “This research reveals principles by which CRC mutations could cause cancer.”
Chromosomes are made of long DNA strands compressed around nodes of protein called nucleosomes; when DNA is compressed, the genes in that area are turned off. Some CRCs, called disassembly CRCs, act as motors that unwind sections of DNA chains, making genes active for a given cell process. Another type, called assembly CRCs, rewinds the DNA chain, recompressing it when the process is complete. The unwind-rewind cycle is repeated continuously throughout a cell’s life.
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