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Can quantum mechanics explain why DNA mutates spontaneously?

The two strands of DNA’s famous double helix are linked together by subatomic particles called protons – the nuclei of hydrogen atoms – which provide the glue that binds molecules called bases together. These so-called hydrogen bonds are like the rungs of a twisted ladder which constitutes the double helix structure discovered in 1952 by James Watson and Francis Crick from the work of Rosalind Franklin and Maurice Wilkins.

Normally, these DNA bases (called A, C, T, and G) follow strict rules on how they bind: A always binds to T and C always binds to G. This strict pairing is determined by the shape of the molecules, fitting them together like pieces of a jigsaw puzzle, but if the nature of the hydrogen bonds changes slightly, it can cause the pairing rule to break, causing the wrong bases to bond together and thus mutation. Although predicted by Crick and Watson, only now has sophisticated computer modeling been able to quantify the process accurately.

The team, part of Surrey’s research program in the exciting new field of quantum biology, have shown that this change in the bonds between DNA strands is much more widespread than previously thought. . Protons can easily jump from their usual location on one side of an energy barrier to land on the other side. If this happens just before the two strands are unzipped in the first step of the copying process, the error can traverse the replication machinery in the cell, resulting in what is called DNA mismatch and, potentially , a mutation.

In a paper published this week in the journal Nature Communications Physics, the Surrey-based team at the Leverhulme Quantum Biology Doctoral Training Center used an approach called open quantum systems to determine the physical mechanisms that could cause protons to jump between strands of DNA. But, most intriguingly, is thanks to a well-known, yet almost magical, quantum mechanism called the tunnel effect – similar to a ghost walking through a solid wall – that they manage to break through.

It was previously thought that such quantum behavior could not occur in the hot, humid and complex environment of a living cell. However, the Austrian physicist Erwin Schrödinger had suggested in his 1944 book What is Life? that quantum mechanics can play a role in living systems since they behave quite differently from inanimate matter. This last work seems to confirm Schrödinger’s theory.

In their study, the authors determine that the local cellular environment causes protons, which behave like spread waves, to be thermally activated and encouraged across the energy barrier. In fact, the protons turn out to be continuously and very quickly tunneled between the two strands. Then, when the DNA is cleaved into its separate strands, some of the protons are captured from the wrong side, resulting in an error.

Dr. Louie Slocombe, who performed these calculations during his thesis, explains that: “DNA protons can tunnel along DNA’s hydrogen bonds and modify the bases that encode genetic information. The modified bases are called “tautomers” and can survive DNA cleavage and replication processes, causing “transcription errors” or mutations”.

Dr Slocombe’s work at the Leverhulme Quantum Biology Doctoral Training Center in Surrey has been supervised by Professor Jim Al-Khalili (Physics, Surrey) and Dr Marco Sacchi (Chemistry, Surrey) and published in Communications Physics.

Professor Al-Khalili comments:

“Watson and Crick speculated on the existence and significance of quantum mechanical effects in DNA more than 50 years ago, however, the mechanism has been largely overlooked.”

Dr Sacchi continues: “Biologists generally expect tunneling to play a significant role only at low temperatures and in relatively simple systems. Therefore, they tended to ignore quantum effects in DNA. With our study, we believe we have proven that these assumptions do not hold.

Reference: Slocombe L, Sacchi M, Al-Khalili J. An open quantum systems approach for proton tunneling in DNA. Nat Comms Phys. 2022;5(1):109. doi: 10.1038/s42005-022-00881-8.

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