According to Phys.org, scientists from Oxford’s Radcliffe Department of Medicine have achieved the most detailed view yet of DNA folding inside living cells, mapping the human genome down to a single base pair resolution using a new technique called MCC ultra. The research team led by Professor James Davies published their findings in the journal Cell under the title “Mapping chromatin structure at base-pair resolution unveils a unified model of cis-regulatory element interactions.” Doctoral researcher Hangpeng Li led the experimental work that revealed how the genome’s control switches are physically arranged, while collaboration with Professor Rosana Collepardo-Guevara at Cambridge confirmed the folding patterns through computer simulations. This breakthrough provides scientists with a powerful new tool to understand how genetic differences lead to diseases like heart disease, autoimmune disorders, and cancer, opening fresh routes for drug discovery by showing exactly how genes are controlled at the molecular level.
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Why this matters
Here’s the thing about genetics – we’ve known the sequence of our 3 billion DNA “letters” for over two decades, but we’ve been mostly blind to how they actually fold and function inside cells. Think about it: each cell packs about 2 meters of DNA into a space one-hundredth of a millimeter across. That’s some serious origami.
Until now, scientists could only see these interactions at relatively low resolution. We knew DNA loops and bends to bring distant sections together, but we couldn’t see the fine details. This new technique changes everything because more than 90% of disease-linked genetic changes occur not in the genes themselves, but in the regulatory “switch” regions that control them. Basically, we’ve been looking at the wiring diagram without understanding how the switches actually connect.
What they found
The Oxford team discovered that cells use electromagnetic forces to bring DNA control sequences to the surface, where they cluster into “islands” of gene activity. These structures were previously invisible, but they appear to be fundamental to how cells read their genetic instructions.
And here’s where it gets really interesting: the computer simulations from Cambridge confirmed that these folding patterns arise naturally from the physical properties of DNA and its packaging proteins. So it’s not random – there’s an underlying physical logic to how our genetic material organizes itself. This gives us a completely new model of gene regulation that could explain why certain genetic variations lead to disease while others don’t.
Real-world impact
So what does this actually mean for medicine? Well, we’re talking about a fundamental shift in how we understand genetic diseases. When you can see exactly how DNA folding brings regulatory switches into contact with genes, you can start to understand why a particular mutation might break that connection.
Professor Davies put it perfectly: “This changes our understanding of how genes work and how things go wrong in disease.” We’re no longer just looking at DNA sequences – we’re seeing the physical architecture that determines which genes get turned on and off. That’s huge for drug discovery because it gives us new targets. Instead of just trying to fix broken genes, we might be able to fix how they’re regulated.
The research paper, available at Cell, represents what could be a turning point in molecular genetics. We’re finally getting a molecular-level view of how our genetic code actually functions in three dimensions. And that’s something that could benefit every field from cancer research to autoimmune diseases.
