Challenges
Datasets
Workspaces
Papers
Discussions
Leaderboard
Log inSign up
Challenges
Datasets
Workspaces
Papers
Discussions
Leaderboard
Blog
Job Board
Q3AS

© 2026 Aqora Quantum S.A.S.

TermsPrivacyLegal Notice

arXiv:1206.2085 · AIP conference proceedings

A proposal on quantum histone modification in gene expression

Liaofu Luo

Published Jan 1, 2012• 6 citations
arXivHTMLPDF

Abstract

A quantum mechanical model on histone modification is proposed. Along with the methyl / acetate or other groups bound to the modified residues the torsion angles of the nearby histone chain are supposed to participate in the quantum transition cooperatively. The transition rate W is calculated based on the non-radiative quantum transition theory in adiabatic approximation. By using W's the reaction equations can be written for histone modification and the histone modification level can be calculable from the equations, which is decided by not only the atomic group bound to the modified residue, but also the nearby histone chain. The theory can explain the mechanism for the correlation between a pair of chromatin markers observed in histone modification. The temperature dependence and the coherence-length dependence of histone modification are deduced. Several points for checking the proposed theory and the quantum nature of histone modification are suggested as follows: 1, The relationship between lnW and 1/T is same as usual protein folding. The non-Arhenius temperature dependence of the histone modification level is predicted. 2, The variation of histone modification level through point mutation of some residues on the chain is predicted since the mutation may change the coherence-length of the system. 3, Multi-site modification obeys the quantum superposition law and the comparison between multi-site transition and single modification transition gives an additional clue to the testing of the quantum nature of histone modification.

DOI
10.1063/1.4756456

Related papers

Quantum Tunneling of the Methyl Group During DNA Histone Methylation: a Quantum Computational Model

Mohammed Osama Alrashdan, Abdallah Barjas Qaswal, Hala Miqdadi +23 more

Histone methylation is one of the molecular mechanisms of epigenetics in which a methyl group or more can be added to the DNA histone proteins. Histone methylation can alter gene expression and thus the overall cellular function. The transfer of the methyl group from the donor AdoMet to the lysine residue of the histone can be mediated via classical transfer or quantum tunneling. In the present study, we aim to explore the role of quantum tunneling in histone methylation compared with the classical transfer of methyl groups. Our results indicate that quantum tunneling provides a wide range of lifetimes for methylated histones between 1.56 x 10-13 s and 1.97 x 10118 s according to the energy of the methyl group and the number of transferred methyl groups. In addition, the tunneling delay time of the methyl group is within a fraction of a picosecond, which is a reasonable time and consistent with the time required for molecular transitions. Our results showed that quantum tunneling favors hypo-methylated histones because the ratio between the lifetimes of the reversed and forward reactions τ_(Q_r )/τ_(Q_f ) equals 1, while classical transfer favors hyper-methylated histones because the same ratio for the classical transfer τ_(C_r )/τ_(C_f ) can range from 4.73 x 108 to 9.6 x 104, depending on the number of transferred methyl groups. However, the ratio is between (1- 4.73 x 108) when either the classical or the quantum transfer is dominant during either the forward or reversed reactions. Moreover, temperature and enzymatic dynamics are important factors that can modulate the lifetime of methylation states.

Biointerface Research in Applied Chemistry•Aug 14, 2026•0 citations

Quantum conformational transition in biological macromolecule

Liaofu Luo

The conformational change of biological macromolecule is investigated from the point of quantum transition. A quantum theory on protein folding is proposed. Compared with other dynamical variables such as mobile electrons, chemical bonds and stretching-bending vibrations the molecular torsion has the lowest energy and can be looked as the slow variable of the system. Simultaneously, from the multi-minima property of torsion potential the local conformational states are well defined. Following the idea that the slow variables slave the fast ones and using the nonadiabaticity operator method we deduce the Hamiltonian describing conformational change. It is proved that the influence of fast variables on the macromolecule can fully be taken into account through a phase transformation of slow variable wave function. Starting from the conformation- transition Hamiltonian the nonradiative matrix element is calculated in two important cases: A, only electrons are fast variables and the electronic state does not change in the transition process; B, fast variables are not limited to electrons but the perturbation approximation can be used. Then, the general formulas for protein folding rate are deduced. The analytical form of the formula is utilized to study the temperature dependence of protein folding rate and the curious non-Arrhenius temperature relation is interpreted. The decoherence time of quantum torsion state is estimated and the quantum coherence degree of torsional angles in the protein folding is studied by using temperature dependence data. The proposed folding rate formula gives a unifying approach for the study of a large class problems of biological conformational change.

arXiv:1301.2417•Jan 11, 2013•0 citations

Is the Viral Genome Quantum Mechanical?

Ramakrishna Podila, Prosanta Pal

We explore a quantum mechanical framework for modeling mutation dynamics in viral genomes. Motivated by experimental observations, such as interference-like mutation patterns and an inverse relationship between genome size and per-site mutation rate, we represent the viral genome as a superposition state in a high-dimensional Hilbert space, and model mutations as quantum operators acting on this state. This is not a microscopic theory of replication but an effective, physically inspired model aimed at capturing non-classical features such as interference and entanglement in sequence evolution. We introduce structured mutation operators diagonal, random, and spatially correlated, and study their action on quantum sequence states using numerical simulations. Correlated operators with phase structure produce interference patterns in mutation probabilities, analogous to the electron double-slit experiment. Entangled mutation dynamics, modeled via cluster-state-like correlations, alter the scaling behavior of the per-site mutation rate with genome size. We show that while classical models predict a constant per-site mutation rate for small genomes, entangled models yield size-dependent rates that decrease as L −α , where α > 0 reflects the strength of correlation. This matches trends observed in RNA viruses with genomes below ∼ 30 kb. Finally, we propose two experimental tests: (1) detection of replication-speed-dependent interference fringes using modified viral polymerases, and (2) ensemble-level coherence signatures measurable by nuclear magnetic resonance spectroscopy. Our results offer a testable hypothesis that quantum correlations may influence mutation dynamics in viral genomes below 30 kb in size.

•Apr 7, 2025•0 citations

Is the Viral Genome Quantum Mechanical?

Prosanta Pal, Ramakrishna Podila

We explore a quantum mechanical framework for modeling mutation dynamics in viral genomes. Motivated by experimental observations, such as interference-like mutation patterns and an inverse relationship between genome size and per-site mutation rate, we represent the viral genome as a superposition state in a high-dimensional Hilbert space, and model mutations as quantum operators acting on this state. This is not a microscopic theory of replication but an effective, physically inspired model aimed at capturing non-classical features such as interference and entanglement in sequence evolution. We introduce structured mutation operators diagonal, random, and spatially correlated, and study their action on quantum sequence states using numerical simulations. Correlated operators with phase structure produce interference patterns in mutation probabilities, analogous to the electron double-slit experiment. Entangled mutation dynamics, modeled via cluster-state-like correlations, alter the scaling behavior of the per-site mutation rate with genome size. We show that while classical models predict a constant per-site mutation rate for small genomes, entangled models yield size-dependent rates that decrease as \( L^{-\alpha} \), where \( \alpha > 0 \) reflects the strength of correlation. This matches trends observed in RNA viruses with genomes below \(\sim 30\) kb. Finally, we propose two experimental tests: (1) detection of replication-speed-dependent interference fringes using modified viral polymerases, and (2) ensemble-level coherence signatures measurable by nuclear magnetic resonance spectroscopy. Our results offer a testable hypothesis that quantum correlations may influence mutation dynamics in viral genomes below 30 kb in size.

•May 22, 2025•0 citations

A Quantum Model on Chemically-Physically Induced Pluripotency in Stem Cells

Liaofu Luo

A quantum model on the chemically and physically induced pluripotency in stem cells is proposed. Based on the conformational Hamiltonian and the idea of slow variables (molecular torsions) slaving fast ones the conversion from the differentiate state to pluripotent state is defined as the quantum transition between conformational states. The transitional rate is calculated and an analytical form for the rate formulas is deduced. Then the dependence of the rate on the number of torsion angles of the gene and the magnitude of the rate can be estimated by comparison with protein folding. The reaction equations of the conformational change of the pluripotency genes in chemical reprogramming are given. The characteristic time of the chemical reprogramming is calculated and the result is consistent with experiments. The dependence of the transition rate on physical factors such as temperature, PH value and the volume and shape of the coherent domain is analyzed from the rate equation. It is suggested that by decreasing the coherence degree of some pluripotency genes a more effective approach to the physically induced pluripotency can be made.

arXiv:1309.7546•Sep 29, 2013•1 citation

Quantum Decoherence and Quantum-Holographic Information Processes: From Biomolecules to Biosystems

Dejan I. Raković, M. Dugić, M.B. Plavšić +3 more

Our recently proposed quantum approach to biomolecular recognition processes is hereby additionally supported by biomolecular Resonant Recognition Model and by quantum-chemical theory of biomolecular non-radiative resonant transitions. Previously developed general quantumdecoherence framework for biopolymer conformational changes in very selective ligandproteins/ target-receptors key/lock biomolecular recognition processes (with electron-conformational coupling, giving rise to dynamical modification of many-electron energy-state hypersurface of the cellular quantum-ensemble ligand-proteins/target-receptors biomolecular macroscopic quantum system, with revealed possibility to consider cellular biomolecular recognition as a Hopfield-like quantum-holographic associative neural network) is further extended from nonlocal macroscopicquantum level of biological cell to nonlocal macroscopic-quantum level of biological organism, based on long-range coherent microwave excitations (as supported by macroscopic quantum-like microwave resonance therapy of the acupuncture system) - which might be of fundamental importance in understanding of underlying macroscopic quantum (quantum-holographic Hopfieldlike) control mechanisms of embryogenesis/ontogenesis and morphogenesis, and their backward influence on the expression of genes.

Materials science forum•Jul 1, 2006•12 citations
A quantum mechanical model on histone modification is proposed. Along with the methyl / acetate or other groups bound to the modified residues the torsion angles of the nearby histone chain are supposed to participate in the quantum transition cooperatively. The transition rate W is calculated based on the non-radiative quantum transition theory in adiabatic approximation. By using W's the reaction equations can be written for histone modification and the histone modification level can be calculable from the equations, which is decided by not only the atomic group bound to the modified residue, but also the nearby histone chain. The theory can explain the mechanism for the correlation between a pair of chromatin markers observed in histone modification. The temperature dependence and the coherence-length dependence of histone modification are deduced. Several points for checking the proposed theory and the quantum nature of histone modification are suggested as follows: 1, The relationship between lnW and 1/T is same as usual protein folding. The non-Arhenius temperature dependence of the histone modification level is predicted. 2, The variation of histone modification level through point mutation of some residues on the chain is predicted since the mutation may change the coherence-length of the system. 3, Multi-site modification obeys the quantum superposition law and the comparison between multi-site transition and single modification transition gives an additional clue to the testing of the quantum nature of histone modification.
Histone methylation is one of the molecular mechanisms of epigenetics in which a methyl group or more can be added to the DNA histone proteins. Histone methylation can alter gene expression and thus the overall cellular function. The transfer of the methyl group from the donor AdoMet to the lysine residue of the histone can be mediated via classical transfer or quantum tunneling. In the present study, we aim to explore the role of quantum tunneling in histone methylation compared with the classical transfer of methyl groups. Our results indicate that quantum tunneling provides a wide range of lifetimes for methylated histones between 1.56 x 10-13 s and 1.97 x 10118 s according to the energy of the methyl group and the number of transferred methyl groups. In addition, the tunneling delay time of the methyl group is within a fraction of a picosecond, which is a reasonable time and consistent with the time required for molecular transitions. Our results showed that quantum tunneling favors hypo-methylated histones because the ratio between the lifetimes of the reversed and forward reactions τ_(Q_r )/τ_(Q_f ) equals 1, while classical transfer favors hyper-methylated histones because the same ratio for the classical transfer τ_(C_r )/τ_(C_f ) can range from 4.73 x 108 to 9.6 x 104, depending on the number of transferred methyl groups. However, the ratio is between (1- 4.73 x 108) when either the classical or the quantum transfer is dominant during either the forward or reversed reactions. Moreover, temperature and enzymatic dynamics are important factors that can modulate the lifetime of methylation states.
The conformational change of biological macromolecule is investigated from the point of quantum transition. A quantum theory on protein folding is proposed. Compared with other dynamical variables such as mobile electrons, chemical bonds and stretching-bending vibrations the molecular torsion has the lowest energy and can be looked as the slow variable of the system. Simultaneously, from the multi-minima property of torsion potential the local conformational states are well defined. Following the idea that the slow variables slave the fast ones and using the nonadiabaticity operator method we deduce the Hamiltonian describing conformational change. It is proved that the influence of fast variables on the macromolecule can fully be taken into account through a phase transformation of slow variable wave function. Starting from the conformation- transition Hamiltonian the nonradiative matrix element is calculated in two important cases: A, only electrons are fast variables and the electronic state does not change in the transition process; B, fast variables are not limited to electrons but the perturbation approximation can be used. Then, the general formulas for protein folding rate are deduced. The analytical form of the formula is utilized to study the temperature dependence of protein folding rate and the curious non-Arrhenius temperature relation is interpreted. The decoherence time of quantum torsion state is estimated and the quantum coherence degree of torsional angles in the protein folding is studied by using temperature dependence data. The proposed folding rate formula gives a unifying approach for the study of a large class problems of biological conformational change.
We explore a quantum mechanical framework for modeling mutation dynamics in viral genomes. Motivated by experimental observations, such as interference-like mutation patterns and an inverse relationship between genome size and per-site mutation rate, we represent the viral genome as a superposition state in a high-dimensional Hilbert space, and model mutations as quantum operators acting on this state. This is not a microscopic theory of replication but an effective, physically inspired model aimed at capturing non-classical features such as interference and entanglement in sequence evolution. We introduce structured mutation operators diagonal, random, and spatially correlated, and study their action on quantum sequence states using numerical simulations. Correlated operators with phase structure produce interference patterns in mutation probabilities, analogous to the electron double-slit experiment. Entangled mutation dynamics, modeled via cluster-state-like correlations, alter the scaling behavior of the per-site mutation rate with genome size. We show that while classical models predict a constant per-site mutation rate for small genomes, entangled models yield size-dependent rates that decrease as L −α , where α > 0 reflects the strength of correlation. This matches trends observed in RNA viruses with genomes below ∼ 30 kb. Finally, we propose two experimental tests: (1) detection of replication-speed-dependent interference fringes using modified viral polymerases, and (2) ensemble-level coherence signatures measurable by nuclear magnetic resonance spectroscopy. Our results offer a testable hypothesis that quantum correlations may influence mutation dynamics in viral genomes below 30 kb in size.
We explore a quantum mechanical framework for modeling mutation dynamics in viral genomes. Motivated by experimental observations, such as interference-like mutation patterns and an inverse relationship between genome size and per-site mutation rate, we represent the viral genome as a superposition state in a high-dimensional Hilbert space, and model mutations as quantum operators acting on this state. This is not a microscopic theory of replication but an effective, physically inspired model aimed at capturing non-classical features such as interference and entanglement in sequence evolution. We introduce structured mutation operators diagonal, random, and spatially correlated, and study their action on quantum sequence states using numerical simulations. Correlated operators with phase structure produce interference patterns in mutation probabilities, analogous to the electron double-slit experiment. Entangled mutation dynamics, modeled via cluster-state-like correlations, alter the scaling behavior of the per-site mutation rate with genome size. We show that while classical models predict a constant per-site mutation rate for small genomes, entangled models yield size-dependent rates that decrease as L−α L^{-\alpha} L−α, where α>0 \alpha > 0 α>0 reflects the strength of correlation. This matches trends observed in RNA viruses with genomes below ∼30\sim 30∼30 kb. Finally, we propose two experimental tests: (1) detection of replication-speed-dependent interference fringes using modified viral polymerases, and (2) ensemble-level coherence signatures measurable by nuclear magnetic resonance spectroscopy. Our results offer a testable hypothesis that quantum correlations may influence mutation dynamics in viral genomes below 30 kb in size.
A quantum model on the chemically and physically induced pluripotency in stem cells is proposed. Based on the conformational Hamiltonian and the idea of slow variables (molecular torsions) slaving fast ones the conversion from the differentiate state to pluripotent state is defined as the quantum transition between conformational states. The transitional rate is calculated and an analytical form for the rate formulas is deduced. Then the dependence of the rate on the number of torsion angles of the gene and the magnitude of the rate can be estimated by comparison with protein folding. The reaction equations of the conformational change of the pluripotency genes in chemical reprogramming are given. The characteristic time of the chemical reprogramming is calculated and the result is consistent with experiments. The dependence of the transition rate on physical factors such as temperature, PH value and the volume and shape of the coherent domain is analyzed from the rate equation. It is suggested that by decreasing the coherence degree of some pluripotency genes a more effective approach to the physically induced pluripotency can be made.
Our recently proposed quantum approach to biomolecular recognition processes is hereby additionally supported by biomolecular Resonant Recognition Model and by quantum-chemical theory of biomolecular non-radiative resonant transitions. Previously developed general quantumdecoherence framework for biopolymer conformational changes in very selective ligandproteins/ target-receptors key/lock biomolecular recognition processes (with electron-conformational coupling, giving rise to dynamical modification of many-electron energy-state hypersurface of the cellular quantum-ensemble ligand-proteins/target-receptors biomolecular macroscopic quantum system, with revealed possibility to consider cellular biomolecular recognition as a Hopfield-like quantum-holographic associative neural network) is further extended from nonlocal macroscopicquantum level of biological cell to nonlocal macroscopic-quantum level of biological organism, based on long-range coherent microwave excitations (as supported by macroscopic quantum-like microwave resonance therapy of the acupuncture system) - which might be of fundamental importance in understanding of underlying macroscopic quantum (quantum-holographic Hopfieldlike) control mechanisms of embryogenesis/ontogenesis and morphogenesis, and their backward influence on the expression of genes.