Quantum frontiers: Quantum biology 42 physicsworld.com Nature’s quantum subways Jim Al-Khalili describes the new experiments and theories exploring whether quantum tunnelling of hydrogen causes mutations in our DNA Physics World March 2013 Shutterstock/Lonely
physicsworld.com “Some of us should venture to embark on a synthesis of facts and theories, albeit with secondhand and incomplete knowledge of some of them – and at the risk of making fools of ourselves.” So said Erwin Schrödinger in 1943 upon his foray from quantum physics into genetics. He would soon back up these words with his hugely influential 1944 book, What is Life?, in which he predicted that genetic information is stored within an aperiodic crystal – an idea that would be confirmed by Francis Crick and James Watson less than a decade later when they discovered the structure of the double helix. Today, a small but increasing number of us would echo Schrödinger’s sentiments, even though the case has yet to be made conclusively for a causal link between some of the weirder aspects of quantum mechanics and biology. It is certainly true that although many examples can be found in the literature dating back half a century, there is still no widespread acceptance that quantum mechanics – that baffling yet powerful theory of the subatomic world – might play a crucial role in biological processes. Of course, biology is, at its most basic, chemistry, and chemistry is built on the rules of quantum mechanics in the way atoms and molecules behave and fit together. But biologists have (until recently) been dismissive of the counterintuitive aspects of the theory – they feel it to be unnecessary, preferring their traditional balland-stick models of the molecular structures of life. Likewise, physicists have been reluctant to venture into the messy and complex world of the living cell. Why should they when they can test their theories far more cleanly in the controlled environment of the physics lab, where they at least feel they have a chance of understanding what is going on? But now, experimental techniques in biology have become so sophisticated that the time is ripe for testing a few ideas familiar to quantum physicists. Sticking together Of all the quantum processes suggested as playing a role in biology – which include quantum coherence, superposition and entanglement – one of the least contentious and best studied is quantum tunnelling. This is the mechanism whereby a subatomic particle, such as an electron, proton or even a larger atomic nucleus, does not have enough energy to punch through a potential barrier (essentially a force field), but instead behaves as a spread-out fuzzy entity that can leak through the barrier and so occasionally find itself on the other side. This phenomenon is familiar in physics and is the mechanism responsible for radioactive decay and nuclear fusion. Quantum tunnelling is also well known in chemistry, for example in the form of hydrogen tunnelling in hydrogen-bonded dimer molecules, such as benzoic acid. It turns out that even in biology it is now well established that electrons quantum tunnel in enzymes, allowing certain chemical processes to speed up by several orders of magnitude. But one particular question that I, and others, have been exploring over the past few years is whether quantum tunnelling of hydrogen nuclei (protons) in the form of a hydrogen bond Quantum frontiers: Quantum biology has a role to play in one of the most important processes in molecular biology: DNA mutation. Hydrogen bonds are stronger than Van der Waals forces but weaker than ionic and covalent bonds, being a happy medium that hold certain organic molecules together. Crucially, they are strong enough to help build stable structures, but not so strong that they cannot be broken, which is why the structures can be rearranged into new configurations. The hydrogen bond is also responsible for stabilizing proteins and for modulating the speed and specificity of chemical reactions. In physical terms, the hydrogen bond can be described as a proton trapped in a double, often asymmetric, finite potential well. The two potential minima exist because the proton is happiest being close to one or other of the two atoms at each end of the bond, with an energy barrier in the middle, which the proton can only get over classically if given sufficient energy. To understand the proton’s behaviour we need to map the shape of this well, or potential energy surface, very accurately. This is no trivial matter as its shape depends on many variables. Not only is the bond typically part of a large complex structure consisting of hundreds or even thousands of atoms, it is also usually immersed in a warm bath of water molecules and other chemicals. Moreover, molecular vibrations, thermal fluctuations, chemical reactions initiated by enzymes and even UV or ionizing radiation can all affect the behaviour of the bond both directly and indirectly. In addition to all this, and what is of most interest here, is that the small mass of the proton means it is able to behave quantummechanically and very occasionally tunnel through the potential barrier from one well to the other (see for example the 2011 paper by Angelos Michaelides and colleagues at University College London – Proc. Natl Acad. Sci. 108 6369). This discussion is certainly relevant to DNA, which consists of two nucleotide chains wrapped around each other in a double helix. They are held together and stabilized by hydrogen bonds, which link the base pairs: adenine to thymine (A–T) and cytosine to guanine (C–G). If we consider the A–T base pair, which is held together by two hydrogen bonds, then as a result of the different possible positions of the hydrogen atoms that form the bonds, two different structures are possible. Normally, the protons form what is called the canonical (keto) structure of the base pair (figure 1), but occasionally they can be found shifted across to the opposite sides of the hydrogen bonds to form the rare tautomeric (enol) form. After their landmark paper, which was published 60 years ago next month, Watson and Crick’s interests quickly turned to the biological implications of the double-helix structure and in a follow-up paper of 1953 they suggested that spontaneous mutation – a change in the genetic code, for example from ATCAT to ATCAC – may be caused by a base taking on its higher-energy, rarer, tautomeric form. A decade later, the Swedish physicist Per-Olov Löwdin boldly proposed that the tautomeric base pair that leads to a mutation is formed through double proton transfer, with each particle quantum tunnelling through the barrier separating the two asymmetric potential wells Jim Al-Khalili is a theoretical nuclear physicist and holds a chair in public engagement in science at the University of Surrey, UK. He is also a broadcaster and author whose latest book is Paradox: the Nine Greatest Enigmas in Physics published by Bantam Press, e-mail j.al-khalili@ surrey.ac.uk Physics World March 2013 43
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