Artur Ruppel

Artur Ruppel

Experimental biophysicist
Institut Pasteur, Paris

I am an engineer by training, and I started my scientific journey in Grenoble, studying the mechanics of force transmission between epithelial cells. There I became fascinated by how cells build structures many times their own size during development, and so in Montpellier I turned to the elementary unit of tissue morphogenesis: the T1 transition, in which cells exchange neighbours. The next step was the scale of the whole tissue. In 2025 I joined Institut Pasteur to address tissue mechanics and organisation in cancer, where the tight homeostatic control of a healthy tissue goes awry.

Throughout, my approach has stayed the same: I build minimal tissues, from two cells to several thousand, in which forces and shapes can be measured directly. Micropatterning sets the geometry, optogenetics lets me switch contractility on and off, traction force microscopy gives me the forces, and segmentation and tracking follow every cell, with simulations alongside to make sense of the measurements. What occupies me now is mechanical heterogeneity. The cells of a tumour differ in stiffness, contractility and adhesion, and I want to understand how these differences between individual cells set the state of the tissue as a whole.

Portrait of Artur Ruppel

Research

Mechanical heterogeneity in cancer cell collectives

Current work · Institut Pasteur · with Sandrine Etienne-Manneville

No two cells in a tissue are the same. In a tumour the differences are stark: soft cells next to stiff ones, regions that flow next to regions that are stuck. Physics has models for how a collective of cells can flow like a fluid or arrest like a solid, and these models make a prediction I find remarkable: a mixture does not behave like the average of its components, and where the different cells sit can matter more than how many of them there are. I want to know whether this holds in a living tissue, and how the mechanical differences between individual cells set the state of the whole.

Drawing of a solid-like tissue, with short cell velocity arrows, and a fluid-like tissue, with long ones
A tissue can be solid-like, with cells that barely move, or fluid-like, with cells that flow past one another. Arrows show cell velocity.

To find out, I build tissues in which the heterogeneity can be controlled. I take two populations of glioblastoma cells that differ in a single component of the cytoskeleton, vimentin, and study them alone and mixed, from pairs of cells to tissues of several thousand. At every scale I measure the shapes, movements and forces of the individual cells alongside the behaviour of the tissue as a whole, and I run simulations of deformable cells, in which the kind and the arrangement of heterogeneity can be controlled more directly, to connect the two.

Left: wild-type and vimentin-knockout glioblastoma cells cultured together on a circular micropattern. Centre: segmented cells and nuclei, coloured by population. Right: simulation of forty deformable cells confined in a disc.

The elementary unit of tissue rearrangement

CRBM, Montpellier · with François Fagotto, Martial Balland and Lisa Manning

A tissue changes shape by letting its cells exchange neighbours. This process, cell intercalation or the T1 transition, is how a tissue can deform a great deal and still hold together. Two mechanisms are known to drive it: the junction between two cells contracts, or cells migrate in between their neighbours. Theory says that every exchange has to cross an energy barrier, and that the height of this barrier decides whether the tissue flows or arrests. The trouble is that in a tissue the exchanges are mechanically coupled to one another, and so the barrier of a single event had never been measured.

Drawing of four cells exchanging neighbours: two cells that touch along a junction lose contact and the other two come into contact
A neighbour exchange, or T1 transition, in its simplest form: four cells, one junction. The two cells that share it separate, the other two come into contact.
Drawing of the two mechanisms of cell intercalation: cells migrating in between their neighbours, and a junction contracting until it vanishes and a new one expands
The two mechanisms of cell intercalation. Left: cells migrate in between their neighbours. Right: the junction between two cells contracts until it vanishes and a new junction expands between the other two. Reviewed in Huebner and Wallingford, Developmental Cell (2018).

We isolated a single event by confining four cells on a cross-shaped micropattern. These quadruplets exchange neighbours on their own, and the forces can be followed throughout: interfacial tensions from the shapes of the cells, migratory forces from traction force microscopy. We found that both tension and migration drive the exchange, in MDCK epithelial cells as well as in Xenopus mesoderm cells. From the distribution of junction lengths we obtained an effective energy landscape with a cusp at the point of exchange, just as vertex models predict. And when we elongated the pattern, the barrier rose in proportion to the strain and exchanges became rarer: geometry controls how readily cells rearrange.

From embryo to quadruplet: a Xenopus embryo, a tissue explant dissociated into single cells, seeded on a cross-shaped micropattern, forming a quadruplet
From embryo to quadruplet. A piece of mesoderm is cut from a Xenopus embryo and dissociated into single cells, which are seeded on cross-shaped micropatterns. Four cells fill a pattern.

Ruppel, Misiak et al., Nature Physics (2026)

A cell quadruplet during a neighbour exchange. Left: traction forces exerted on the substrate. Right: segmented cells with the contact angles from which interfacial tensions are inferred.
All 21 Xenopus quadruplets of the published data, in the viewer of my lab notebook: segmented cells and traction forces over time. Use the sliders to move through time and between quadruplets. Open full page · Data (CC BY 4.0)

Force propagation between epithelial cells

LIPhy, Grenoble · with Martial Balland, Thomas Boudou and Ulrich Schwarz

Cells in a tissue coordinate what they do through the forces they exert on one another. Mechanical signals travel faster than biochemical ones and can have much the same effect. Yet nobody had followed the chain of events quantitatively: one cell generates a force, the force crosses the contact between the cells, and the neighbour responds. This was the question of my PhD.

Drawing of a cell contracting inside a tissue, its neighbours marked with question marks, reduced to a pair of cells on a micropattern
How do cells respond to the forces of their neighbours? One cell in a tissue contracts; the question is reduced to a pair of cells.

We built a minimal system in which the chain can be followed: two MDCK epithelial cells on an H-shaped micropattern. With optogenetics we made one cell contract on demand, and with traction force microscopy we measured how its neighbour responded. The neighbour, it turned out, actively contracts in its own right. A single cell of the same size behaves differently: its actin network flows instead of building up stress. How strongly the neighbour responds depends on how the cell pair is mechanically and structurally polarised, which we could set through the shape of the micropattern. The response is strongest when the polarisation is perpendicular to the direction in which the force travels, and the same holds in small tissues of a few hundred cells. And so active response and cellular organisation allow mechanical signals to keep their strength as they travel from cell to cell.

Drawing of the three tools: an H-shaped micropattern that yields a cell doublet, light that makes one cell contract, and marker beads in a soft substrate that move when the cell pulls
The three tools of the experiment. Micropatterns give doublets of the same shape and size; optogenetics makes one cell contract on demand; marker beads in the soft substrate move when the cells pull, and their displacement gives the forces.

Ruppel, Wörthmüller et al., eLife (2023)

One cell of a doublet is photoactivated (blue lines mark the light pulses). Left: actin with traction forces. Centre: traction stress map. Right: strain energy of the activated half (blue) and of the neighbouring half (orange). From Ruppel, Wörthmüller et al., eLife (2023), CC BY.
The published data in the viewer of my lab notebook: 29 doublets with the left cell activated, 42 doublets with both cells activated and 41 single cells with the left half activated. Light pulses come once a minute between minute 20 and 30; the readout marks them. Switch between actin, displacement, traction and stress under Layers. Open full page · Data (CC0)

Publications

First author

  1. A minimal in vitro assay for cell intercalation highlights the importance of interfacial tension and migratory forces

    A. Ruppel*, V. Misiak*, S. Arzash, D. Selma-Herrador, T. Boudou, M. L. Manning†, F. Fagotto†, M. Balland†

    Nature Physics (2026) · doi:10.1038/s41567-026-03311-6

  2. napariTFM: An open-source tool for traction force microscopy and monolayer stress microscopy

    A. Ruppel†, D. Wörthmüller, M. Balland, F. Fagotto

    PLOS Computational Biology 22, e1014045 (2026) · doi:10.1371/journal.pcbi.1014045

  3. An open-source Python tool for traction force microscopy on micropatterned substrates

    A. Ruppel†, V. Misiak, M. Balland†

    Bio-protocol 15, e5156 (2025) · doi:10.21769/BioProtoc.5156

  4. Force propagation between epithelial cells depends on active coupling and mechano-structural polarization

    A. Ruppel*, D. Wörthmüller*, V. Misiak, M. Kelkar, I. Wang, P. Moreau, A. Méry, J. Révilloud, G. Charras, G. Cappello, T. Boudou, U. S. Schwarz, M. Balland

    eLife 12, e83588 (2023) · doi:10.7554/eLife.83588

Collaborations

Force measurements, and sometimes simulations, for the questions of others.

  1. Remodeling of cadherin contacts in embryonic mesenchymal tissues during differential cell migration

    D. Rozema, C. Fagotto-Kaufmann, A. Ruppel, P. Lasko, F. Fagotto

    Developmental Cell 60, 2915–2930 (2025) · doi:10.1016/j.devcel.2025.06.009

    I repeated the key experiments with a myosin construct expressed at lower levels (MHCIIA-StayGold). They confirmed that myosin is recruited to the cortex next to the contact in the last phase of detachment, after the cadherins have condensed, and that the construct leaves cortical tension and migration speed unchanged.

  2. A crosstalk between adhesion and phagocytosis integrates macrophage functions into their microenvironment

    M. Depierre, A. Mularski, A. Ruppel, C. Le Clainche, M. Balland, F. Niedergang

    iScience 28, 112067 (2025) · doi:10.1016/j.isci.2025.112067

    I helped set up the traction force measurements and interpret them.

  3. An EpCAM/Trop2 mechanostat differentially regulates collective behaviour of human carcinoma cells

    A. Aslemarz, M. Fagotto-Kaufmann, A. Ruppel, C. Fagotto-Kaufmann, M. Balland, P. Lasko, F. Fagotto

    The EMBO Journal 44, 75–106 (2025) · doi:10.1038/s44318-024-00309-9

    I measured traction and cell-cell forces of MCF7 doublets with and without EpCAM or Trop2, and ran Cellular Potts simulations of spheroid spreading. The altered tensions alone account for the different spreading phenotypes.

  4. Light-driven biological actuators to probe the rheology of 3D microtissues

    A. Méry, A. Ruppel, J. Révilloud, M. Balland, G. Cappello, T. Boudou

    Nature Communications 14, 717 (2023) · doi:10.1038/s41467-023-36371-w

    I took part in designing the experiments, in the measurements and in the analysis.

  5. A mechano-osmotic feedback couples cell volume to the rate of cell deformation

    L. Venkova, A. S. Vishen, S. Lembo, N. Srivastava, B. Duchamp, A. Ruppel, A. Williart, S. Vassilopoulos, A. Deslys, J. M. Garcia Arcos, A. Diz-Muñoz, M. Balland, J.-F. Joanny, D. Cuvelier, P. Sens, M. Piel

    eLife 11, e72381 (2022) · doi:10.7554/eLife.72381

    I measured the traction forces of cells in control conditions and under ROCK and Arp2/3 inhibition, to go with the volume measurements of the team.

  6. Interplay between extracellular matrix stiffness and JAM-A regulates mechanical load on ZO-1 and tight junction assembly

    A. J. Haas, C. Zihni, A. Ruppel, C. Hartmann, K. Ebnet, M. Tada, M. S. Balda, K. Matter

    Cell Reports 32, 107924 (2020) · doi:10.1016/j.celrep.2020.107924

    I helped set up the traction force measurements and analyse them.

* equal contribution · † corresponding author

Software

I build the software I need for my research and make it available on my GitHub when it is ready to be used by others.

napariTFM

Published · open source

A napari plugin for traction force microscopy and monolayer stress microscopy. It covers the complete analysis, from bead displacements to traction forces and internal stresses, for single cells and monolayers, on single images or time series.

A. Ruppel et al., PLOS Computational Biology 22, e1014045 (2026) · Paper · Code · Test data

ITASC

Ready to use · open source

A napari plugin that segments and tracks cells in dense, highly motile monolayers, where automatic methods break down. It combines Cellpose and Ultrack with interactive correction adapted from EpiCure, and gives every cell and its nucleus one identity that holds across the whole recording.

Documentation · Code

Private tools

These form my own working environment. Some have a public repository, but none has been tested on other machines. I am happy to share them on request.

Select a logo to see what the tool does.

Curriculum vitae

Research

  1. 2025 – present

    Postdoctoral researcher, Institut Pasteur, Paris

    Cell Polarity, Migration and Cancer Unit, Sandrine Etienne-Manneville

  2. 2022 – 2025

    Postdoctoral researcher, CRBM, CNRS and University of Montpellier

    Group of François Fagotto

  3. 2018 – 2022

    PhD in biophysics, LIPhy, CNRS and Université Grenoble Alpes

    Thesis: Optogenetic interrogation of intercellular propagation of force signals. Supervised by Martial Balland and Thomas Boudou. Defended 6 May 2022.

Education

  1. 2016 – 2018

    MSc in biomedical engineering, Grenoble INP – Phelma

    Double degree with TU Darmstadt

  2. 2012 – 2018

    MSc in electrical engineering, Technische Universität Darmstadt

    Specialisation in micro- and precision engineering

Supervision

  1. 2021

    Vladimir Misiak, master's student, LIPhy, Grenoble

    Co-supervised with Martial Balland. Co-first author of Ruppel, Misiak et al., Nature Physics (2026).

Talks

  1. 2026

    Seminar, group of Abdul Barakat

    LadHyX, École Polytechnique, Palaiseau

  2. 2026

    Paris Postdoc Seminar

    Institut Jacques Monod, Paris

  3. 2026

    QBio seminar

    Institut Pasteur, Paris

  4. 2025

    Cytoskeleton Day

    Paris

  5. 2025

    Theory seminar, group of Pierre Sens

    Institut Curie, Paris

  6. 2022

    Cell and Developmental Systems

    Arolla, Switzerland

  7. 2019

    French Optogenetics Club

    Paris

Posters and workshops

  1. 2026

    PhysCell

    Egmond aan Zee, Netherlands · poster

  2. 2023

    CellMech

    Marseille · poster

  3. 2023

    Physics of Living Systems

    Dresden, Germany · poster

  4. 2021

    MiFoBio summer school

    Hyères, France · workshop and poster

  5. 2021

    Cell la vie

    Online · poster

  6. 2021

    EMBO workshop ImmunoBiophysics

    Online · poster

  7. 2019

    CellMech

    Milan, Italy · poster

  8. 2018

    Mechanobiology of Polarized Cells, summer school

    Les Houches, France · poster

Languages

German (native), English and French (fluent).

Contact

Email
artur.ruppel@pasteur.fr
Address
Institut Pasteur, 25–28 rue du Docteur Roux, 75015 Paris, France
Code
github.com/ArturRuppel
ORCID
0000-0002-2541-8257
Google Scholar
Artur Ruppel
Bluesky
@arturruppel.bsky.social
LinkedIn
linkedin.com/in/artur-ruppel-6b4b8a131