Welcome

This is the homepage of the Heltberg Group

We are based at the University of Copenhagen and are researching how living cells use physical principles to regulate signaling, decision-making, and gene expression.

Cells constantly respond to their environment and internal signals, relying on dynamic regulation to control processes like growth, repair, and adaptation. We are particularly interested in how time-dependent behaviors—such as oscillations, fluctuations, and chaos—shape biological outcomes. While such dynamics are observed across many systems, their functional role remains poorly understood.

At the same time, cells organize many key processes in space using biomolecular condensates—droplet-like structures formed without membranes. These condensates provide a way to concentrate molecules and create distinct reaction environments, and they appear to be deeply integrated with cellular regulation.

Our group recently uncovered that oscillatory dynamics can influence condensate formation, suggesting a deeper link between temporal signals and spatial organization. This opens the door to a broader understanding of how cells coordinate complex behavior in both time and space.

We are a theoretical group, grounded in statistical physics and dynamical systems theory, aiming to uncover the fundamental principles behind cellular regulation. Our models are designed to be testable and predictive, and we work in close collaboration with experimental groups to ensure that our theories are rooted in biological reality.

By combining physics, mathematics, and biology, we aim to shed light on how cells coordinate complex decisions across time and space—potentially revealing universal principles of regulation in living systems.

Biomolecular Condensates

Background

Biomolecular condensates are membrane-less organelles that play a fundamental role in organizing cellular components. These structures form through the physical process of liquid-liquid phase separation. Inside the cell, these structures are dynamic, as they can quickly be formed and dissolved. However, the mechanisms by which cells regulate and control this process remain an open question. My research applies concepts from theoretical physics to predict and understand the behavior of biological condensates. In particular, we explore how the cell can control the timing and positioning of condensates - and how this interacts with the dynamical protein concentration of specific components.

Project

Research Direction 1: Condensates in Dynamic Fields

Our research focuses on the interplay between dynamic signaling and phase transitions in the DNA damage response. When cells experience DNA damage, they rapidly form specialized sub-compartments, or foci, at the break sites to coordinate repair. A well-known hallmark of this response is the oscillatory behavior of the transcription factor p53, yet how these temporal dynamics influence the physical organization of repair machinery has remained unclear. In this work, we develop a theoretical framework describing foci formation as a droplet condensation process, and uncover how oscillations in p53 concentration—with specific frequency and amplitude—can enhance repair efficiency. These oscillations prevent Ostwald ripening, helping to maintain multiple repair foci and ensuring effective spatial distribution of repair proteins. Guided by our model, we confirm experimentally that the oscillatory dynamics of p53 optimize the DNA repair process.

Research Direction 2: Functional Impact of Condensate Formation on DNA Repair Efficiency

A major focus of our work is to understand the functional relevance of condensate formation during DNA repair. We hypothesize that condensates enhance repair by enriching critical proteins at damage sites, facilitating faster and more efficient assembly of repair complexes. Through molecular dynamics simulations, we investigate how condensates influence molecular interactions and polymer formation essential for repair. We also perform experimental studies to correlate condensate formation with DNA repair accuracy and cell survival. This research aims to establish the direct physiological role of condensates in promoting effective DNA repair.

Research Direction 3: Fusion and Fission Dynamics of Nucleated Condensates

We study the fusion and fission behavior of nucleated condensates formed at specific DNA sites during cellular responses such as DNA repair. While freely diffusing condensates readily fuse, the dynamics are more complex when condensates are anchored to nucleation sites. We hypothesize that fission, while absent in passive systems, may occur for site-bound condensates at rates determined by the balance between surface tension and diffusion at the nucleation sites. Using stochastic reaction-diffusion models and analytical theory, we investigate how chemical activity at nucleation sites affects condensate stability and fragmentation. Experimentally, we collaborate to map the position of DNA damage sites using CRISPR technology, testing how genomic distance influences condensate fusion. This research aims to reveal the fundamental principles governing the stability, fusion, and fission of condensates in living cells.

Research Direction 4: Negative Feedback Loops in the Presence of Phase Separation

We explore how phase separation alters the dynamics of biological feedback loops. Traditional biochemical models assume reaction rates scale linearly with reactant concentrations, but phase separation fundamentally changes this relationship by restricting reactant accessibility. When one component undergoes phase separation, the effective inhibition scaling changes, potentially promoting oscillations in systems that would otherwise remain stable. Through theoretical analysis and reaction-diffusion simulations, we study how phase-separated networks behave differently from well-mixed systems, focusing on how altered scaling laws drive oscillatory behavior. Our research provides a new framework for understanding negative feedback, oscillations, and network stability in the context of spatial organization and molecular condensation.

Research Direction 5: Pyrenoid fission in Cell Division

In this project, we explore a physical model for pyrenoid division by introducing an energy barrier that bisects the domain. This setup effectively redirects material laterally in order to minimize the system’s free energy. The framework we use is based on the Cahn–Hilliard equation with a spatially dependent free energy, capturing phase separation dynamics under imposed heterogeneity.

Our core assumption is that particle motion is driven purely by diffusion, consistent with the principles of the Cahn–Hilliard model. While the imposition of an arti cial energy barrier may initially seem idealized, incorporating a slowly varying potential—as recently implemented in our simulations—provides a more realistic and continuous approximation.

We also assume the system is incompressible, re ecting the uid nature of the pyrenoid matrix. Incompressibility implies that external pressure alters the shape of the domain without changing its volume, driving material redistribution without bulk compression. Consequently, we model the system using a xed-volume thermodynamic ensemble, consistent with our prior studies. This approach provides a foundational model for understanding how physical constraints and energy landscapes can drive symmetry breaking and division in biological condensates like the pyrenoid.

Dynamics of Protein Concentrations

Project

Research Direction 1: Decoding p53 Dynamics and Cell Fate Decisions

Our group investigates how cells use dynamic signaling to make critical cell fate decisions, focusing on the DNA damage response as a model system. In this context, the tumor suppressor p53 plays a central role, coordinating cellular outcomes such as cell cycle arrest or apoptosis through its function as a transcription factor. Under normal conditions, p53 levels are kept low by regulatory proteins like Mdm2, but upon DNA damage, activation of ATR or ATM kinases leads to p53 stabilization and activation. We study how different types of DNA damage induce distinct p53 dynamics, ranging from sustained oscillations to large transient pulses, and how these temporal patterns influence downstream cellular responses. Despite significant progress, it remains largely unknown how cells interpret these dynamic signals and translate them into specific phenotypic outcomes. An emerging hypothesis is that bimolecular condensate formation—especially at sites of DNA repair—could modulate the temporal dynamics of p53, adding an additional layer of regulation. Our research aims to uncover the molecular mechanisms that detect, interpret, and integrate p53 dynamics, providing new insights into how cells control fate decisions under stress.

Research Direction 2: Dynamics, Temperature Control, and Mode-Hopping in NF-kB Signaling

Our group investigates how dynamic and stochastic behaviors in the transcription factor NF-kB regulate immune system responses. Upon stimulation with TNF-α, NF-kB exhibits oscillatory nuclear localization, but how environmental factors like temperature modulate these oscillations remains poorly understood. Through a combination of experiments and mathematical modeling, we show that the period of NF-kB oscillations shortens with increasing temperature, and we accurately capture this behavior using a model incorporating temperature-dependent reaction rates derived from statistical physics. This model predicts that gene expression patterns shift at different temperatures, favoring the upregulation of high-affinity genes at higher temperatures.

We also explore how periodic external inputs influence NF-κB dynamics, discovering that NF-κB can undergo cellular mode-hopping—spontaneous transitions between distinct frequency modes under periodic TNF stimulation. Through stochastic simulations, we reveal that noise facilitates mode-hopping across all conditions, while chaotic dynamics lead to rapid, erratic transitions. Interestingly, experimental data match the regime where noise, rather than chaos, drives mode-hopping, suggesting a mechanism by which different NF-kB-dependent genes can be selectively activated over time.

Research Direction 3: The Role of coupled oscillators in Biological Regulation

Our group investigates how complex dynamical behaviors emerge from coupled oscillators in biological systems and contribute to cellular function and regulation. By studying coupled oscillators, we explore how increasing interaction strength leads from entrainment and controlled synchronization to mode hopping and chaotic dynamics. These behaviors have been observed across a range of biological systems, yet their functional roles remain largely unexplored. We focus on understanding how dynamic patterns, particularly in key regulators like p53 and NF-κB, influence downstream gene expression during cellular stress responses. Using controlled external perturbations to systematically tune oscillatory behavior, we aim to uncover how different dynamic regimes—steady states, oscillations, and chaos—can optimize biological processes for flexibility, robustness, and adaptation. Our work seeks to advance a new understanding of how dynamic complexity is not merely a byproduct of biological networks, but a functional asset that living organisms may exploit to maintain regulation and resilience.

Research direction 4: How Oscillatory and Chaotic Transcription Factor Dynamics Shape Gene Expression

Our group explores how dynamic fluctuations in transcription factors influence downstream gene regulation. While it is known that transcription factors adjust their activity in response to cellular signals, the impact of oscillatory and chaotic dynamics on gene expression remains poorly understood. We focus on NF-κB, demonstrating how oscillatory stimulation can induce chaotic behavior that reshapes gene expression patterns. Our work shows that chaotic NF-κB dynamics can upregulate families of low-affinity genes, enhance protein complex formation, and improve assembly efficiency, even in the presence of biological noise. Additionally, chaotic signaling generates heterogeneous populations of cell states, offering potential advantages in environments with multiple stresses. Through this research, we reveal new principles for how dynamic regulation can enhance both robustness and adaptability in cellular systems.

Deriving Observables from Single Particles

Background

Our group investigates the physical principles underlying nuclear condensate formation, with a focus on DNA repair and gene silencing. We use single-particle tracking (SPT) to quantify protein motion during the earliest stages of condensate nucleation and apply Hidden Markov Models (HMMs) to extract kinetic states and transitions from experimental trajectories. These analyses are integrated with stochastic simulations and coarse-grained molecular dynamics to model protein dynamics, phase behavior, and spatial organization. We apply this combined approach to diverse systems—from chemically driven nucleation by scaffold proteins to condensates formed by p53 and the polymer-bridging behavior of SIR3—revealing how molecular properties and interactions shape condensate formation, evolution, and function.

Project

Research Direction 1

Our group investigates the early stages of DNA repair condensate formation, with a focus on understanding how small numbers of scaffold proteins nucleate these structures through chemically driven processes. Using advanced live-cell imaging and single-particle tracking (SPT), we quantify the motion and diffusion of individual proteins during the earliest phases of nucleation. We develop novel Hidden Markov Models (HMM) to extract kinetic and spatial information from experimental data, and complement these analyses with molecular dynamics simulations and theoretical models based on free energy landscapes. This combined approach allows us to reveal the fundamental physical mechanisms governing condensate nucleation and the timescales of protein motion within emerging repair foci.

Research Direction 2: The Role of p53 and Its Disordered Regions in Condensate Formation

We study the direct involvement of the tumor suppressor p53 in DNA repair condensate formation, with particular focus on the function of its intrinsically disordered regions (IDRs). Using coarse-grained molecular dynamics simulations, we model how these disordered domains drive condensate assembly and influence the physical properties of repair structures. By analyzing the spatially resolved diffusion of wild-type and mutant p53 proteins, we aim to distinguish between liquid-like and more solid-like condensate states. These insights help us understand how mutations in p53 affect condensate formation and, ultimately, cellular repair efficiency.

Research Direction 3: The Spatiotemporal Evolution of DNA Repair Condensates

Our group examines how the composition and physical properties of DNA repair condensates change over time. Using live-cell imaging, we track the behavior of key repair proteins such as TOPBP1, 53BP1, and p53 to determine whether repair foci are static structures or dynamic, evolving assemblies. To interpret these observations, we perform coarse-grained molecular simulations and stochastic reaction-diffusion modeling, analyzing how the removal or replacement of condensate components affects stability and function. This research provides critical insights into the dynamic regulation of condensates and the mechanisms that govern their formation, maintenance, and dissolution during the DNA damage response.

Research Direction 4: The Role of SIR3 and Polymer Bridging in Gene Silencing

Our group study how the protein SIR3 organizes nuclear foci to maintain stable gene silencing. Using single-particle tracking, we find that the motion of SIR3 is consistent with the polymer bridging model (PBM), where foci are formed by dense networks of specific binding sites rather than by liquid-like phase separation. Through theoretical modeling, we show that polymer-bridged structures naturally slow molecular diffusion, creating physical barriers that delay the access of transcription factors and reinforce silencing. This contrasts with liquid-like foci, which facilitate rapid molecular interactions. Our work suggests that long-lived, stable foci, such as those involved in gene regulation, are best explained by polymer bridging, while dynamic, short-lived foci - such as those in DNA repair - are more likely driven by phase separation.

Dynamics of Neuronal Signaling

Background

Understanding how neural systems transition between functional states is a central challenge in neuroscience. Our group investigates these transitions using biophysical modeling and theoretical frameworks that capture the complex dynamics of neural activity. In one line of research, we study the mechanisms behind sleep-wake transitions, demonstrating that changes in potassium channel conductance can drive a shift from stable, oscillatory sleep states to chaotic dynamics characteristic of wakefulness.

We also investigate dopaminergic signaling in Parkinson’s disease, where we model how different patterns of neuronal denervation impact striatal network activity. This work leads to a proposed compensatory strategy in which remaining neurons upregulate both dopamine release and reuptake to preserve function. In a third direction, we explore how time delays and feedback in coupled neural populations give rise to chimera states and breathing chimeras—patterns that reflect a coexistence of synchrony and desynchronization.

Projects

Dynamics of neurons in the Sleep-Wake transition

One direction of our research focuses on the neural dynamics underlying sleep-wake transitions. While prior studies have highlighted the role of extracellular ion concentration changes in driving these transitions, the intricate coupling between neuronal activity and ion concentrations makes it difficult to disentangle cause and effect in vivo.

To address this, we extend computational models such as the Averaged-Neuron model to explore how intrinsic neuronal properties contribute to brain state transitions. Our work reveals that a reduction in the conductance of calcium-dependent potassium channels—rather than ion concentration shifts alone—can initiate the transition from sleep to wakefulness.

Through this modeling framework, we show that sleep is characterized by stable, self-sustained oscillations, while the quiet and active wakeful states exhibit irregular and chaotic dynamics. We investigate how transitions between these states are modulated by ionic changes, and demonstrate that chaotic dynamics can facilitate smooth, noise-resistant transitions, offering insight into how the brain maintains robustness during state changes.

Dopamine signaling during early stages of Parkinsons Disease

Another key focus of our research is understanding the mechanisms underlying dopaminergic dysfunction in Parkinson’s disease (PD). PD is marked by the progressive loss of dopaminergic neurons, yet the precise triggers of signaling breakdown—and how the brain might compensate—remain poorly understood. The variability in age of onset, progression, and symptoms across patients further complicates our clinical understanding.

To address these challenges, we use biophysical modeling to characterize the dopaminergic landscape of both healthy and denervated striatum. We explore how different patterns of neuronal denervation—based on proposed pathological mechanisms—affect the dynamics of the dopaminergic network. Our work reveals that these patterns can give rise to distinct local and global changes in striatal neuron activity, providing insight into the heterogeneity seen in PD.

Our models suggest a potential compensatory cellular strategy for preserving dopamine signaling: a coordinated upregulation of both dopamine release and reuptake in the remaining neurons. This approach forms the basis for a new conceptual framework to understand impaired dopaminergic signaling in PD.

Chimera States of Neurons

We are also interested in the emergent dynamics of coupled neural populations, with a focus on how time delays and feedback shape collective behavior. Neurons can be broadly classified into two excitability types, each responding differently to inputs, as described by their phase response curves (PRCs). In this line of research, we investigate networks of neural populations with type I excitability connected through delayed interactions and organized in negative feedback loops.

Using a combination of analytical and numerical methods, we analyze the stability of network states in the continuum limit. Our work identifies how delays and coupling strengths—both within and between populations—influence the emergence of synchrony and incoherence. Notably, we discover the existence of chimera states, where coherent and incoherent neural activity coexist, especially under conditions where external coupling dominates internal interactions. These states are particularly intriguing for their robustness to noise, offering insight into real-world brain dynamics.

In regimes with minimal internal coupling and no time delays, we uncover a novel family of breathing chimeras—neutrally stable, periodic orbits that reflect a delicate balance between synchrony and desynchronization. These findings contribute to a deeper understanding of how structured heterogeneity and delays can give rise to rich dynamical phenomena in neural systems.

Physics of Football

Background

Football is a dynamical game, predominantly played in two dimensions. Whereas football is described qualitatively by numeous expterts, the quantification and understanding of the dynamical positioning of the teams and relations between playermovements is still far from understood. Statistics of fixed events (goals, passes etc.) is a well-founded industry, but taking the events into a holistic framework, using all player positions and movements is still to be thoroughly implemented.

Project

Research Direction 1: In-game characterization of all situations

Modern football analysists work on putting each segments of the game into defined chategories based on their tactical framework. It is our ambition to describe the game using algorithms based on mathematical definitions and based on this draw new conclusions about core events in a game of football.

Research Direction 2: Statistical physics of defending

A very important part of a modern football game is to break down an opponent that defends with all players. In a situation like this, defending is a coherent strategy of all players, where in general each player position themselves in relation to their nearest team-mates, the ball and to a some degree the movement of opposition players. In this regard, defending is a question of creating order thereby lowering the entropy of the system. On the contrary, attacking is a question of enhancing the entropy through movements of the ball and the players. My group will use this framework to characterize this part of football through measurements of statistical physics and derive how one can enhance the entropy of a defending side.

About me

My research explores how living cells harness physical principles to respond to their environment and regulate internal processes. During my Ph.D., I investigated how dynamic behaviors—such as oscillations and chaos—in the concentrations of key regulatory proteins can emerge, and how cells may use these dynamics to enhance control and signaling. This work led me to Harvard, where I demonstrated how oscillatory dynamics can be used to uncover the structure of underlying biological networks. My dissertation was awarded the Ph.D. Prize from the Faculty of Science at the University of Copenhagen.

As a postdoctoral researcher at École Normale Supérieure, I developed my independent research profile, focusing on how cells orchestrate DNA repair through phase separation. We published two major studies demonstrating that structures at DNA damage sites are indeed liquid condensates. By developing new mathematical tools, I introduced a novel framework for distinguishing the physical nature of observed condensates.

Returning to Copenhagen as an independent postdoc, I integrated these findings into a new theory explaining how oscillations in the regulatory protein p53 following DNA damage may regulate condensate formation and capture phase transitions in an underlying dynamic field. This theory was experimentally validated by collaborators in Taiwan and published in Cell (forming the foundation of my current research group.

My overall ambition is to understand how living cells apply aspects of physics to control regulation and signalling. In this long-term dream I aim both to derive new relations of physics and to understand how life as we see it today are using physics in the way it is to create an ordered and well-regulated machinery.

In my sparetime I love to spend time with my family. I love to play football and do various kinds of outdoor activities. I also enjoy reading, in particular I am fond of diving into world-history and understand how the big philosophical ideas of mankind have evolved over time. Finally I love spending time with my friends, playing board games, enjoying a beer and taking it easy.

Curriculum Vitae

General Information

Name: Mathias Luidor Heltberg
Birthday: 11th of July 1990, Denmark
Address: Gråstensgade 4, 3. th. 1677 København V
Contact: +45 26191889 / heltberg@nbi.ku.dk
Degree: PhD in physics
Position: Individual postdoctoral researcher in physics

Education

2010-2013: Bachelor in Physics at the University of Copenhagen
2014: Summer student programme at CERN, Geneva.
2014: Research assistant in the department of Neuroscience and Pharmacology, University of Copenhagen.
2014 - 2017: Master in Physics at the University of Copenhagen
2018: Researcher at Harvard Medical School, Lahav Lab, Boston
2017-2019: PhD in Physics at the University of Copenhagen
2019-2021: Postdoc at Institut Curie and Ecole Normale Superieure, Paris
2020: Researcher at Statens Serum Institut (SSI) in the COVID-19 "Expert Group"
2021: Postdoc at Carlsberg reintegration grant.
2021-2024: Lundbeck postdoc fellowship.

Previous work unrelated to research

2017-?: CTO at the startup company NucliRay (www.nucliray.com)
2020: Selected for Entrepreneur First talent programme (Declined)
2004-2014: Football coach and responsible for development for several youth teams on elite level
2012: Worked in the advertisement company Wunderman, Copenhagen
2014: Received UEFA A-license in soccer coaching
2021-?: Football coach for FC Rudersdal playing in Sjællandsserien
2022: Data analyst for FC Nordsjælland Superliga team

Teaching experience

2009-2010: Public school teacher in physics and biology
2015: Lecturer for undergraduate students on statistics and data science (Mekanik 1)
2014-2016: Teaching Assistant in “Applied Statistics”,“Dynamical systems and chaos","Introduction to Classical Mechanics"
2016-2020: Supervised 3 bachelor students, 3 master students and 1 PhD student.
2021: Course responsible: NFYB10019U, Lineær algebra og klassisk mekanik (MatN)
2021: Course responsible: NFYK13011U, Anvendt statistik: Fra data til resultat

Prizes, grants and awards

2019: PhD prize (award for best PhD), University of Copenhagen, Department of Science
2020: Kirstine Meyer Memorial Grant
2021: Carlsberg Reintegration Fellowship
2021: Lundbeck fellowship grant
2023: Carlsberg Semper Ardens grant (Co-recipient)
2024: Berlingske Talent 100

Relevant qualifications

Export in constructing biophysical models using partial differential equations (deterministic and stochastic).
Expert in analysis of large sets of data and parameter estimation (from single molecule level to population dynamics).
Expert in using programming languages MATLAB, Python, ROOT, Fortran, Java and C++.
Experience in government service and generation of applicable results.
Experience in leadership from football clubs and the UEFA A-licence.

Some invited lectures

2015: University of Tokyo, Japan. "Arnold Tongues and Cell Signalling
2015: NCBS Bangalore, India. "Protein Production in E. Coli
2016: Peking University, China. "Arnold Tongues and Cell Signalling
2016: University of Chennai, India. "On Transcription-translation density in E. Coli". Conference on mathematical modelling of biological systems
2017: University of Lille, France. "Modehopping in Coupled Oscillators". Conference on coupled oscillations in biology
2017: Harvard Medical School, USA. "NF-kB Cell Signalling and Modehopping
2017: Stanford University, USA. "NF-kB Cell Signalling and Modehopping
2019: Ecole Normale Superieure, France. "The Physics of Foci Formation
2021: APS annual meeting. "Physics of foci formation".
2022: MIT, USA. "Enhanced DNA repair through droplet formation and p53 oscillations".
2023: Q-Bio Winter school, USA. "Enhanced DNA repair through droplet formation and p53 oscillations".
2023: University of Dresden, Germany. "Enhanced DNA repair through droplet formation and p53 oscillations".

Some public outreach

2016: Fysikkens fremskridt: “Fra molekylære processer til menneskets principper", Invited lecture (Lyngby), https : //issuu.com/f of kbh/docs/kbh − ef teraar − 2016/44
2016: "Men har vi ret til at brokke os?", Feature article (kronik) in Danish Newpaper "Berlingske Tidende".
2016: Naturens byggesten: “Livsprocessernes molekylære maskine”, Invited lecture (Niels Bohr Institute, Copenhagen), https : //issuu.com/f of kbh/docs/low − resc openhagen/9
2017: Nordsjællands Astronomiforening: “Fra molekylære processer til menneskets principper”, Invited lecture (Helsingør, Denmark), https : //novastronomi.wordpress.com/about/aktiviteter−i−nova−2/
2018: "On the Denervation of Dopamine Neurons and Parkinsons Disease”, Nyborg. Part of meeting held by AbbVie on Parkinsons Disease
2018: Den2Radio: “Om livets fysik”, Radio broadcast, http : //den2radio.dk/udsendelser/om − livets − f ysik
2020: https://www.dr.dk/nyheder/viden/kroppen/29-aarige-mathias-elsker-loese-gaader-nu-hjaelper-han-harvard-forskere-med (Main Story of Danish media Danmarks Radio, also part of P1 Morgen)
2020: https://ekstrabladet.dk/plus/krop-og-traening/mathias-vaekker-opsigt-dansk-forsker-taet-paa-at-knaekke-kraeftgaaden/8077883 (Cover Story of Danish newpaper Ekstra Bladet)
2020: "De Ubekendte", Article in Danish Newpaper "Weekendavisen", about the mathematics of Corona modelling.
2020: "https://www.berlingske.dk/danmark/forskerne-kender-dig-kan-spaa-om-effekt-af-smittetiltag", Presentation of Danish COVID-19 model
2020: https://ekstrabladet.dk/plus/taet-paa/mathias-hjerne-er-danmarks-nye-corona-vaaben/8347240
2022: “Overgangen fra klassisk fysik til kvantemekanik”, Invited lecture (Niels Bohr Institute, Copenhagen)
2022: "Cellernes Vitale svingninger", Aktuel Naturvidenskab

Mathias Heltberg

Lukas Wolf Kristensen

I have a background in physics from the University of Copenhagen. In my bachelor thesis, I investigated the role of oscillations in the regulation of cell signaling. My primary interest is the interplay and relationship between biological regulation and statistical mechanics, and I am currently working on how oscillating dynamics within cells can help organize liquid-liquid phase separation. When not doing physics, I enjoy spending my free time birdwatching, cooking, and reading books about history and linguistics.

Emilie Jessen

I hold a bachelor’s degree in physics from the University of Copenhagen, where my bachelor thesis focused on the negative feedback loop between the transcription factor p53 and its inhibitor mdm2, with particular emphasis on the system’s oscillatory behavior. During my master’s studies, I specialized in computational physics, with a strong interest in how computational methods and statistical tools can be used to investigate complex systems. Currently, I am working on modelling the diffusive behaviour of a single particle in the cell nucleus after condensate formation due to DNA damage. In my spare time, I enjoy running or relaxing with a knitting project.

Alessandra Lucchetti

I studied Physics in Padua, Italy, and then moved to Copenhagen in 2018 for my Master’s Degree in Bio-physics. I obtained my PhD Degree at the Niels Bohr Institute in 2023 with Prof. Mogens H. Jensen and Mathias S. Heltberg, where I investigated the emergence of complex behaviours in biological oscillators, ranging from the synchronisation of neurons to the role of oscillating transcription factors in regulating DNA repair.

I then continued my research in the group as a postdoc, where I became more and more interested in how cells exploit the phenomenon of liquid phase separation to achieve a robust spatiotemporal regulation of its internal components.

Currently I am exploring the molecular mechanisms regulating the dynamics of the pyrenoid, a CO2-fixing organelle found in most green alghe, that behaves like a liquid droplet. I employ finite different method simulations of the Chan-Hiliard-Navier Stokes (CHNS) equation coupled with reaction kinetics of the pyrenoid components.

In my spare time, I sing in an international choir and engage in many different arts and crafts projects.

Malthe Nordentoft

I chose to study physics because I saw it as a powerful way to understand the world around us. After completing my studies, I had the privilege of joining the Heltberg group as a PhD student, where I could apply my knowledge to real-world research.

My main research area is biophysics. Here I mainly use principles from statistical physics and dynamical systems theory to gain deeper insights into complex biological phenomena. My work has included studying how dendrites gain specificity through the extracellular space, how circadian cell-to-cell coupling affects individual cell cycles, and how free energy potentials can be determined at the micron scale within individual cells.

Outside of research, I enjoy running orienteering races in the forests surrounding Copenhagen.

Funding

Contact

Email: heltberg@nbi.ku.dk
Phone: +45 26 19 18 89
Github: github.com/MathiasHeltberg

I have abandoned social media - but that makes it easier to contact me in these direct forms :)

Address:
Niels Bohr-bygningen
Jagtvej 155
2200 Copenhagen N
Denmark