Using the force landscape of an active solid to predict plastic deformation Non-active disordered solids feature quasilocalized excitations that control plasticity, similar to crystal lattice defects, and these excitations can be identified via harmonic or anharmonic analyses...

Check out his manuscript and preprint on the thesis work: arxiv.org/abs/2603.11425
arxiv.org/abs/2407.13939
with more to come in the next few months!

Big day for the Manning Research Lab: Tyler Hain is defending his Ph.D. thesis, “Mapping the Rigid Landscapes of Disordered Networks and Active Solids.” Yay, Tyler! events.syracuse.edu/event/disser....

3 Faculty Members Named AAAS Fellows Duncan Brown, Kevin Crowston and Lisa Manning are the first trio from Syracuse to earn the prestigious science honor in a single year.

Thanks to all the students, postdocs, and collaborators over the past 15 years that really did the work that this AAAS Fellowship celebrates. Happy to share it with all of you! news.syr.edu/2026/03/26/3...

Tanya Chhabra, Impact of tunable interactions on emergent behavior in a random field Ising model with feedback,
March 19th, 12:48–1:00 p.m. | Convention Center, Bluebird 2A
Physics of Learning and Adaptation III | MAR-U57

Somiealo Azote epse Hassikpezi, A Predictive Model for Coupling Cell Division Orientation to Tissue Mechanics During Epithelial Morphogenesis,
March 19th, 8:36–8:48 a.m. | Convention Center, Bluebird 2B
Mechanics of Cells and Tissues IV | MAR-S58

Lisa Manning, Rigidity transitions in confluent and mesenchymal biological tissues,
March 17th, 5:54–6:30 p.m. | Convention Center, Bluebird 1A
Rigidity Transitions in Biological Tissues and Materials | MAR-J54

Tyler Hain, Using the force landscape of an active solid to predict plastic deformation,
March 17th, 2:36–2:48 p.m. | Convention Center, Bluebird 2G
Active Matter II | MAR-G63M

Rajendra Negi, Mechanobiological Regulation of Symmetry Breaking During Zebrafish Embryogenesis: Interplay of Myosin Activity, Mechanical Forces, and External Flows,
March 16th, 5:30–5:42 p.m. | Convention Center, Bluebird 2E
Morphogenesis I | MAR-C61

Alex Grigas, Porous mesenchymal tissue as a fluid under tension,
March 16th, 1:24–1:36 p.m. | Convention Center, Bluebird 2E
Mechanics of Cells and Tissues I | MAR-B61

Kelly Aspinwall, Parameterization of the critically rigid manifolds of vertex models,
March 16th, 1:00–1:12 p.m. | Convention Center, Bluebird 2E
Mechanics of Cells and Tissues I | MAR-B61

Manning research group represents at the APS March meeting (aka Global Summit)! I am so proud of all the great work that will be presented by current students and postdocs from our research group. Here's a time-ordered list of talks, please check them out if you're in Denver this week!

And also, what are all those oriented cell divisions doing to the tissue mechanics? stay tuned...

Dynamic regulation of tissue fluidity controls skin repair during wound healing During skin wound repair, the basal cell layer transitions from a solid-like homeostatic state to a fluid-like state that allows tissue remodeling during repair and then progressively returns to a sol...

Previous work from the Sprinzak and Campas/Simons/Blanpain labs suggest some interesting possible paths forward… www.cell.com/cell/fulltex... , www.cell.com/developmenta...

Future work: A key remaining open question on the physics side is precisely how this tissue-stiffness-dependent Notch activation is triggered – how do only a subset of cells (exactly the right number, perhaps not too close together) decide to commit?

Notch activity itself is gated by tissue stiffness and basal layer density/cell shape. This generates an elegant self-organizing feedback loop where delamination is directly link to the abundance and packing of basal layer stem cells, explaining the robustness of epithelial self-renewal.

The basement membrane and the basal layer of the tissue are substantially stiffer and less fluid-like at E15.5 and E16.5 compared to E14.5.

Cell state commitment in the basal layer activates Notch signaling. At E15.5 and E16.5 a population of Notch positive cells emerges that share characteristics of both basal and suprabasal cells, and also exhibit cell shapes and protein localization patterns consistent with cells that delaminate.

Next, we wonder how cells decide to commit to delamination at these later stages, so as to have precisely the right number of cells moving up to keep the basal layer in homeostasis (not over- nor under-populated).

At E14.5, only small changes to a cell’s mechanics (x-axis) are needed to get a cell to robustly delaminate (fraction of delaminating cells, y-axis -> 1). At E15.5 and E16.5, a very large change to cell mechanics is required to get a cell to delaminate.

We can use an Arrhenius approximation to extract the magnitude of the mechanical barrier to delamination from the rates of cell delamination. We find a large mechanical barrier emerges at E15.5 (and the barrier is small before that).

These changes -- predicted by fitting the model to experimental cell and tissue geometries -- are corroborated by observations of protein expression levels and localization.

At later stages (E15.5), the interaction with the basement membrane becomes wetting (negative sigma_b), and the heterotypic apical tension and tissue stiffness both increase, with further tissue stiffening even later at (E16.5).

The results are that at earlier stages (E14.5) the basal layer is soft (small delta s) with small heterotypic tension at the apical side (small sigma_a) and a positive, repulsive interaction with the basement membrane (sigma_b).

We used another set of data collapses to predict how each observable depends on model parameters, allowing us to use an overconstrained solver to determine the vertex model parameter that best match our experimental observations!

Three vertex model parameters control those observables – the cell stiffness parameterized in terms of a cell shape (delta s), a wetting tension with the basement membrane (sigma_b), and a heterotypic interfacial tension at the apical side of basal cells interacting with suprabasal cells (sigma_a).

In both simulations and experiments, we can measure 4 quantities – apical angle of basal cells, orientation of later interfaces with respect to the basement membrane, overall roughness of the basal-suprabasal interface, and height of basal cells.

To quantify how the magnitude of the barrier changes across developmental stages, we developed a method to match 3D vertex model parameters to cell- and tissue scale observables.

A vertex model simulation data collapse demonstrates that the rate at which cells are able to move upwards depends on a precise combination of the apical and basal tensions of the committed cell, as well as on the stiffness of surrounding cells.

We use a stratified 3D vertex model to demonstrate that the barrier prevents cells from freely moving across these compartments, unless a committed cell changes its mechanical properties.

At later stages perpendicular divisions are suppressed, and cells must commit to delamination and change their mechanical properties dramatically in order to move upward from the basal layer.