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Posts by Julia Eckert

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📢Preprint: Positional information (PI) and information flows in dynamic tissues.
Our mathematical framework quantifies, from data, how the coupled stochastic dynamics of cell positions and properties preserve, degrade and generate PI. @alex-plum.bsky.social www.biorxiv.org/content/10.6...

8 hours ago 32 11 0 0
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some really cool stuff here : www.biorxiv.org/content/10.6...
withe the amazing @gaellerecher.bsky.social

15 hours ago 5 2 1 1

A real computational tour de force by @ericneiva.bsky.social, carried out as Marie Skłodowska-Curie postdoctoral fellow in the team, now published in the Journal of Computational Physics: urlr.me/AuzK86

Congratulations, Eric!

@cnrsbiologie.bsky.social
Grateful to @ec.europa.eu for funding support

1 day ago 19 6 0 0

Hearts have topological defects. By treating the mouse myocardium as a 3D nematic, we found disclination lines threading through it. In situs inversus hearts, twist must match structural chirality for contraction to work, as found by quantifying the nematic chirality.
biorxiv.org/content/10.6...

3 days ago 16 5 1 0

Amazing work! Congratulations! 🥳

5 days ago 1 0 0 0

Topological defects and coherent myocardial chirality shape torsional heart contraction www.biorxiv.org/content/10.64898/2026.04...

5 days ago 1 2 0 0

Just published in @science.org 🚀

By controlling how cells align, we show that living nematic tissues can be programmed to generate forces and fold into predictable 3D shapes.

A new platform for tissue engineering and the design of smart active materials! 🫆

www.science.org/doi/10.1126/...

5 days ago 79 32 8 2
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Pricoupenko, N., Marsigliesi, F., Marcq, P., Blanch-Mercader, C., & Bonnet, I. (2024). Src kinase slows collective rotation of confined epithelial cell monolayers. Soft Matter, #EpithelialMechanics doi.org/10.1039/D4SM...

6 days ago 9 5 0 0
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How can we learn tissue mechanics directly from cell patterns and images?

In our new preprint, we introduce VertAX, a differentiable vertex-model framework in JAX for simulating epithelia, inferring parameters, and designing target tissue behaviors.

shorturl.at/PUzT0
1/5

1 week ago 48 22 2 0
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How does an orbiting spherical tissue suddenly break symmetry and sprout invasive strands? We can predict this behavior from the initial morphology!

Hi, I’m @jiwon-kim.bsky.social from @ianywonglab.bsky.social.

1 week ago 36 15 1 2
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Mechanochemical coupling regulates defect dynamics in active nematics Active nematics offer a versatile continuum framework for nonequilibrium collective phenomena, such as collective cell migration and tissue morphogenesis. However, the dynamic evolution of active…

New study on topological defects develops a mechanochemical model integrating morphogen concentration and hydrodynamic flow, reproducing experimental collective motility and revealing viscosity, activity, and alignment strength as key factors governing defect-mediated transport.

1 week ago 4 3 0 0
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PREPRINT ALERT !!!
Excited to share our #reptile #embryo cryopreservation method optimised on peri-gastrulation veiled chameleon embryos! This lays the foundation for functional studies & reptile #conservation efforts!
#devbio #squamates #evodevo

www.biorxiv.org/content/bior...

2 weeks ago 25 9 3 2
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@lsprahl.bsky.social and Ronald Canlla in the lab just published a detailed study on remote-controlled epithelial budding morphogenesis. We can direct budding, tubule elongation, and perhaps branching in human kidney organoids via a light-activated RET receptor.

www.biorxiv.org/content/10.6...

2 weeks ago 22 8 2 2

A non-invasive approach for understanding localized force generation in 3D tissues

www.biorxiv.org/content/10.6...

2 weeks ago 2 1 0 0
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Mosaic gastruloids reveal a temporal restriction for developmental cell competition - Nature Cell Biology Frenster et al. utilize mosaic mouse gastruloids as a model of cell fitness and competition, identifying a temporal window between primed pluripotency and early gastrulation during which cell competit...

🥳 I am happy to share our latest manuscript published in @natcellbio.nature.com We use #Gastruloids to study #CellCompetition during early mammalian development and find not only that this is highly pronounced in our system but also tightly restricted in time. (1/12) www.nature.com/articles/s41...

2 weeks ago 69 22 6 0
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Rozman, J., & Yeomans, J. M. (2024). Cell Sorting in an Active Nematic Vertex Model. Physical review letters, 133(24), 248401. #EpithelialMechanics
buff.ly/ZSBkCtc

3 weeks ago 6 1 0 0
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I'm happy to present our new tool, EpiCure, a napari plugin to ease correction of segmentation and tracking of epithelia movies, developed in @devstempasteur.bsky.social

3 weeks ago 91 34 2 2
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Since #durotaxis was described >25 years ago, most studies report cells migrating from soft → stiff

New work from my team at @ub.edu (in collaboration with D. Odde's lab) suggests we may have been missing the point all along...

🔥 Check out our new preprint here 👇
www.biorxiv.org/content/10.6...

3 weeks ago 34 19 4 2

Transient contractility attenuation reprograms epithelial cells into a protrusion-driven state that drives tissue fluidization www.biorxiv.org/content/10.64898/2026.03...

3 weeks ago 3 1 0 0

So proud to share my paper on collective chemotaxis and force coordination in epithelial and mesenchymal cells, developed in the Mayor Lab and now published in JCB. Deeply grateful for everything I learned from Xenopus NC and the amphibian world, where adaptation is everything🐸

2 months ago 20 6 0 0
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New piece on the mechanics of squamous epithelial shape transition highlighting the role of tensile forces, force transmission by Dumpy & elastic resistance by the ECM in the developing wing. Terrific work from Stefan Harmansa @morphomechanics.bsky.social with Alex Erlich🍾👏:

tinyurl.com/2p58b3w3

3 weeks ago 38 16 0 0

From Sensor Design to Force Maps: A Systematic Evaluation of FRET-based Vinculin Tension Sensors www.biorxiv.org/content/10.64898/2026.03...

3 weeks ago 6 4 0 0

I am happy to share that our paper is now available online at Advanced Science @wiley.com

advanced.onlinelibrary.wiley.com/doi/epdf/10....

4 weeks ago 16 6 1 0
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This is why we love #CalciumSignaling

Look how mechanical damage triggers long range Ca2+ waves in this plant !!
By @annalisabellandi.bsky.social, who is now around here ;)

Full www.science.org/doi/10.1126/... @science.org #microscopy #cell #mechanobiology 🧪🔬

1 month ago 192 57 3 3
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Activities - GreenTE Activities Webinars ”MechanoBioTalks – Mechanics, Materials and Living Matter” is a webinar series supported by the GreenTE consortium and organized […]

A new webinar series is born - ''MechanoBioTalks - Mechanics, Materials and Living Matter", to bring together and inspire researchers interested in biomechanics, biophysics and biology across different kingdoms of life. Join us!

For info and registration visit green-te.nl/activities/

2 months ago 30 21 1 0

Wonderful thread by @inesfournon.bsky.social on cell extrusion in sea anemones 👇

4 weeks ago 2 0 1 0
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Logic of optimal collective migration in heterogeneous tissues www.biorxiv.org/content/10.64898/2026.03...

1 month ago 2 1 0 1
Fig. 1. Basic steps of cell migration. (a) Mesenchymal cell migration. Cells are attached to the extracellular matrix (ECM) via integrins and focal adhesions (FA). Actin polymerization at the leading edge extends filamentous actin (F-actin) protrusions inducing a front-rear polarization. New FA adhesions attach the protrusions to the ECM followed by F-actin rearward movement, known as actin retrograde flow. Disassembly of rear FA and myosin II contraction at the back of cell generate the pushing force to move the cell forward. (b) Amoeboid cell migration. Cells do not form adhesions with the ECM or other cells. Under confinement, amoeboid cells form membrane blebs, also known as pseudopodia, inducing a front-rear polarization. Actin retrograde flow is initiated by mechanical forces, such as confinement. Myosin II contraction at the back of cell generates the pushing force to move the cell forward.

Fig. 1. Basic steps of cell migration. (a) Mesenchymal cell migration. Cells are attached to the extracellular matrix (ECM) via integrins and focal adhesions (FA). Actin polymerization at the leading edge extends filamentous actin (F-actin) protrusions inducing a front-rear polarization. New FA adhesions attach the protrusions to the ECM followed by F-actin rearward movement, known as actin retrograde flow. Disassembly of rear FA and myosin II contraction at the back of cell generate the pushing force to move the cell forward. (b) Amoeboid cell migration. Cells do not form adhesions with the ECM or other cells. Under confinement, amoeboid cells form membrane blebs, also known as pseudopodia, inducing a front-rear polarization. Actin retrograde flow is initiated by mechanical forces, such as confinement. Myosin II contraction at the back of cell generates the pushing force to move the cell forward.

Fig. 2. MS ion channel families involved in cell migration. (a) Transient receptor potential channels (TRP). TRP channels form 6 transmembrane (TM) domains. TM 1-2 are represented in cyan, TM 3-4 in orange and TM 5-6 in magenta. The pore forming domain is formed between TM5 and TM6. Each subfamily of TRP channels contains unique domains in the cytoplasmic N- and C- termini. TRPC channels have three ankyrin repeats and a coiled-coil domain in the N-terminus. A TRP domain, which has gating functions, a calmodulin and IP3R binding domains are localized in the C-terminus. TRPV channels have six ankyrin repeats in the N-terminus. A TRP domain, a calmodulin and PIP2 binding domains are localized in the C-terminus. (b–b′) Piezo1 channels. (b) Each Piezo1 channel has at least 26 TM regions and up to 40 TM domains. The TM domains form three defined structures, known as blades. Each blade is colour coded in cyan, orange and magenta for easier representation. The carboy-terminal extracellular domain (CED) is located directly on top of the pore forming domain and is important for ion selectivity (Zhao et al., 2016). (b′) Due to its large size, a Piezo1 channel induces a small curvature to the plasma membrane, when force is applied the plasma membrane is stretched, thereby opening the Piezo1 channel.

Fig. 2. MS ion channel families involved in cell migration. (a) Transient receptor potential channels (TRP). TRP channels form 6 transmembrane (TM) domains. TM 1-2 are represented in cyan, TM 3-4 in orange and TM 5-6 in magenta. The pore forming domain is formed between TM5 and TM6. Each subfamily of TRP channels contains unique domains in the cytoplasmic N- and C- termini. TRPC channels have three ankyrin repeats and a coiled-coil domain in the N-terminus. A TRP domain, which has gating functions, a calmodulin and IP3R binding domains are localized in the C-terminus. TRPV channels have six ankyrin repeats in the N-terminus. A TRP domain, a calmodulin and PIP2 binding domains are localized in the C-terminus. (b–b′) Piezo1 channels. (b) Each Piezo1 channel has at least 26 TM regions and up to 40 TM domains. The TM domains form three defined structures, known as blades. Each blade is colour coded in cyan, orange and magenta for easier representation. The carboy-terminal extracellular domain (CED) is located directly on top of the pore forming domain and is important for ion selectivity (Zhao et al., 2016). (b′) Due to its large size, a Piezo1 channel induces a small curvature to the plasma membrane, when force is applied the plasma membrane is stretched, thereby opening the Piezo1 channel.

Fig. 3. Role of MS ion channels in cell migration. (a) Actin protrusions. MS ion channels can regulate the extension of actin-based protrusions through PI3K signalling. Ca2+ binding to PI3K leads to the activation of several Rac1-GEFs, including P-Rex1 and SWAP-70, Vav1, Sos1. Rac1-GEFs mediate the transition from inactive Rac1-GDP to Rac1-GTP, leading to actin polymerization and protrusion extension. (b) RhoA activation. The Ca2+ sensitive Pyk2 kinase is activated after MS ion channel opening. Pyk2 activates PDZ-RhoGEF which mediates the transition from inactive Rho-GDP to Rho-GTP, leading to Myosin II phosphorylation. Global Myosin II contraction leads to inhibition of cell migration. (c) Chemotaxis. The presence of a chemoattractant agent leads to re-localization of TRPC1 and TRPC6 MS ion channels to the direction of the chemoattractant signal. Localized Ca2+ can regulate actin remodelling via PI3K or induce Ca2+ flickers at the leading edge of the cell, promoting directional cell migration. (d) Focal adhesion (FA) disassembly. MS ion channels regulate FA disassembly via calpain, a Ca2+ dependant protease that mediates FA degradation. Restricted calpain activity at the rear of the cell mediates specific FA disassembly at the back of the cell, promoting cell migration. (e) Yap/Taz nuclear localization. Piezo1 activation is correlated with Yap translocation from the cytoplasm to the nucleus, leading to Yap mediated gene transcription. However, the biochemical signals downstream of Piezo1 have not been identified yet. Dashed line represents unknown signalling proteins.

Fig. 3. Role of MS ion channels in cell migration. (a) Actin protrusions. MS ion channels can regulate the extension of actin-based protrusions through PI3K signalling. Ca2+ binding to PI3K leads to the activation of several Rac1-GEFs, including P-Rex1 and SWAP-70, Vav1, Sos1. Rac1-GEFs mediate the transition from inactive Rac1-GDP to Rac1-GTP, leading to actin polymerization and protrusion extension. (b) RhoA activation. The Ca2+ sensitive Pyk2 kinase is activated after MS ion channel opening. Pyk2 activates PDZ-RhoGEF which mediates the transition from inactive Rho-GDP to Rho-GTP, leading to Myosin II phosphorylation. Global Myosin II contraction leads to inhibition of cell migration. (c) Chemotaxis. The presence of a chemoattractant agent leads to re-localization of TRPC1 and TRPC6 MS ion channels to the direction of the chemoattractant signal. Localized Ca2+ can regulate actin remodelling via PI3K or induce Ca2+ flickers at the leading edge of the cell, promoting directional cell migration. (d) Focal adhesion (FA) disassembly. MS ion channels regulate FA disassembly via calpain, a Ca2+ dependant protease that mediates FA degradation. Restricted calpain activity at the rear of the cell mediates specific FA disassembly at the back of the cell, promoting cell migration. (e) Yap/Taz nuclear localization. Piezo1 activation is correlated with Yap translocation from the cytoplasm to the nucleus, leading to Yap mediated gene transcription. However, the biochemical signals downstream of Piezo1 have not been identified yet. Dashed line represents unknown signalling proteins.

Many ion channels eg. TRP, Piezo are mechanically sensitive, meaning they can be activated/deactivated by mechanical stimuli such as membrane curvature or substrate stiffness. In this thorough review from the Mayor lab, they discuss how these channels regulate cell migration.
doi.org/10.1016/j.cd...

1 month ago 12 10 0 1
Cell strain-stiffening drives cell breakout from embedded spheroids

arxiv.org/html/2602.08...

1 month ago 3 2 0 0
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Fournon-Berodia, I., Bruderer, N., Christiaen, L., & Steinmetz, P. R. (2025). Epithelial cell extrusion underlies starvation-induced cell loss in a sea anemone. bioRxiv, 2025-12. #EpithelialMechanics
buff.ly/VJknuUe

1 month ago 8 2 0 0