Tiny molecules involved in the DNA's supportive scaffolding -- once thought to be fixed -- go through dynamic and responsive changes to shield against mutations, new research has found.
"The molecules involved in this study are as small to humans as Jupiter is large," said Rory Duncan, Professor at Heriot-Watt University in Scotland.
The finding could be crucial to understanding DNA damage and genome organisation and could impact current thinking on DNA-linked diseases, including cancers.
"The results open new possibilities for investigating how we might protect against DNA mutations that we see in diseases like cancer," said Nick Gilbert, Professor at the University of Edinburgh.
In human cells, DNA is wrapped around proteins to form chromatin.
Chromatin shields DNA from damage and regulates what genetic information can be read -- a process known as transcription.
Researchers showed that a chemical called scaffold attachment factor A (SAF-A) binds to specific molecules known as caRNAs to form a protective chromatin mesh.
For the first time, this mesh was shown to be dynamic, assembling and disassembling and allowing the structure to be flexible and responsive to cell signals.
In addition, loss of SAF-A was found to lead to abnormal folding of DNA and to promote damage to the genome.
SAF-A has previously been shown in mouse studies to be essential to embryo development and its mutations have repeatedly been found in cancer gene screening studies.
The findings, published in the journal Cell, shed light on how chromatin protects DNA from high numbers of harmful mutations, a condition known as genetic instability, the scientists said.
"These findings are very exciting and have fundamental implications for how we understand our own DNA, showing that chromatin is the true guardian of the genome," Gilbert added.