Potentially dangerous genes embedded within human DNA were once thought to be locked down by helpful DNA structures called heterochromatin. A researcher disputes that belief and hopes to change the paradigm even further.
Human chromosomes are made up of DNA, about half of which includes ancient remnants of a type of virus called transposons. Also known as «jumping genes,» transposons have the potential to attack other parts of the genome and cause mutations and damage if they’re ever free to be expressed.
«To keep transposons from disrupting how our genes function, cells create a structure called heterochromatin,» said Keith Maggert, UA associate professor of cellular and molecular medicine and member of the UA Cancer Center.
Heterochromatin, the guardian that basically handcuffs the dangerous transposons in a compact tangle of DNA strand, prevents transposons from being copied or expressed. But researchers are still working to understand the fundamentals of heterochromatin, and much of what is thought is based on assumption, Maggert said.
One assumption was that once heterochromatin formed on a transposon, it was stable, locked up for good. But research done by Maggert and his team suggests that even early on, some cells fail to silence the transposons, and even the silenced ones aren’t completely quiet.
«People thought heterochromatin was good at its job,» said Maggert, lead author on the paper published today in the journal Proceedings of the National Academy of Sciences. «But heterochromatin makes mistakes, and so it slips from time to time, flickering on and off constantly. Each time it drops the ball, we’re at risk, and certain environmental conditions can lead to increased instability.»
It’s Maggert’s ongoing hypothesis that transposons can do their damage as heterochromatin flickers on and off and becomes unstable, allowing for errors in DNA transcription and, ultimately, the emergence of diseases such as cancer. More research is required to confirm this linkage, Maggert stressed.
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