NEW PROGRAM POSTER for EASTER TERM 2026 available!
Don’t forget to subscribe to our newsletter to get all the updates, the links to ZOOM and reminders straight to your inbox
If you wish to share the message, you’re welcome to use our poster! 😉
find our latest updates on BLUESKY: @CamMorphoSeries
11th May 2026: Hanna-Maria Hakkinen (University of Cambridge) & Quentin Vagne (University of Geneva)
Location: online on Zoom and @ level 2 meeting room, Gurdon Institute, Tennis Court Road, Cambridge, CB2 1QN, UK
Hanna-Maria Hakkinen: In vivo nuclear envelope adaptation during cell migration across confining embryonic tissue environments
In physiology and in disease, cells migrate in challenging 3D environment in their native tissue context. Mechanical stresses from the surroundings can cause increased cellular confinement leading to nuclear deformation, and result as loss of nuclear integrity and DNA damage. Despite the increasing understanding of the consequences of mechanical stress in cultured cells, in vivo, the consequences of physical confinement on physiological, developmental cell migration remain largely unexplored. In the Scarpa lab we use the highly migratory zebrafish neural crest (NC) as an in vivo model to address how multipotent embryonic cells respond to physical confinement during developmental migration. By using in vivo live cell imaging approach we found that the NC undergo dramatic nuclear deformations during migration showing a further increase in deformation levels along the embryonic antero-posterior body axis. By measuring the extracellular space along the NC migratory path we found that also the level of tissue confinement increases along the antero-posterior axis. By using complementary genetic and mechanical strategies to ablate the surrounding tissue, we observe a rescue of nuclear deformation in vivo, supporting that NC deformations results from mechanical confinement by the surrounding tissues. Surprisingly, we found that while deformation of the neural crest nucleus causes stretching of the nuclear envelope, it does not cause nuclear envelope rupture or increase DNA damage even upon extreme deformations. Instead, confined migratory neural crest show decreased LaminB2 at the nuclear envelope, suggesting nucleus adaptation during confined migration. In summary, we have established the neural crest as a novel physiological framework uncovering a dynamic adaptation to tissue confinement in vivo.
https://www.linkedin.com/in/hanna-hakkinen
Quentin Vagne : From observations to theoretical predictions: 3D analysis of MDCK epithelial geometry reveals correlated patterns of cell height and skewing, compatible with large scale tension fluctuations.
The tight packing of cells in epithelia guarantees their cohesiveness and impermeability, essential to their functions. Yet, how cells spatially arrange in three dimensions within them is not fully understood.
Here, we segmented the three-dimensional shapes of more than 30 000 cells in MDCK epithelia, grown in hollow spheres of alginate. This setup removes boundary effects and allows to modulate the substrate properties and tissue curvature. We observed that as the tissue proliferates, the cell volume decreases while cell height is relatively conserved, with a value sensitive to the rigidity, curvature, and adhesive strength of the substrate. We also identified large and spatially correlated fluctuations in cell height and cell skewing (defined as the relative difference between apical and basal area) that do not arise from curvature.
To make sense of these observations, I will show how, by coarse-graining a model based on individual cells with apical, cortical, and basal tensions, one can build a fully analytical description of epithelial mechanics in terms of continuous fields of cell density, height, and tilt. I will then show that, under this framework, tensions fluctuations at scales larger than the single cell are sufficient to explain all the experimental observations.
www.linkedin.com/in/quentin-vagne-1a6492b5
8th May 2026: Toru Ishitan (Osaka University, Japan)
Location: online on Zoom
Mechanosensing-driven cell competition ensures robust morphogen gradient formation
Abstract: Morphogen gradients instruct cells to pattern tissues. Although the mechanisms by which morphogens transduce chemical signals have been extensively studied, the roles and regulation of the physical communication between morphogen-receiver cells remain unclear. By zebrafish in vivo imaging, genetic modification, and transcriptome analyses, we reveal that Mechanical communication between morphogen-receiver cells ensures robust morphogen gradient formation. The Wnt/β-catenin–morphogen gradient, which patterns the embryonic anterior-posterior (AP) axis, generates intercellular tension gradients along the AP axis by controlling membrane cadherin levels in zebrafish embryos. This “mechano-gradient” is used for the cell competition–driven correction of noisy morphogen gradients. Naturally and artificially generated unfit cells, producing noisy Wnt/β-catenin gradients, induce local deformation of the mechano-gradients that activate mechanosensitive calcium channel PIEZO1 in the neighboring fit cells, which then secrete Annexin A1 to kill unfit cells. Thus, our study shows the mechano-gradient and the morphogen gradient correction mediated by the mechano-gradient, which is a previously unidentified mechano-chemical intercellular communication mechanism during embryogenesis. This discovery has prompted a re-evaluation of the conventional concept of morphogen systems and provides new insights into intercellular communication mechanisms regulating development, regeneration, and homeostasis.
At this seminar, we will also introduce our latest findings, including the involvement of this mechano-sensing system in the elimination of de novo mutant cells and the prevention of congenital diseases.
@ishitani-lab.bsky.social
8th June 2026: Annis Richardson (Institute of Molecular Plant Sciences, University of Edinburgh, UK)
Location: online on Zoom
Crazy Leaves and Truffula Trees
Plant architecture is determined by the decisions made at meristems. As cells transition from a stem cell fate to a more determinate state, patterns of hormones and gene expression are initiated that lay the foundations of organ development. The hormone auxin plays a key role in regulating organ development. The pathways that decode auxin’s effects are not well understood. Here we present two dominant maize mutants with opposing vegetative phenotypes; Hoja loca1 (Oja1) and Truffula (Trf); both of which have defects in auxin transcriptional response. Oja1 plants often fail to produce leaves, and those that do form can be midribless or tube-shaped. Oja1 is due to a mutation in the highly conserved degron motif of the auxin response repressor ZmIAA28. In contrast, Trf plants develop extra leaves, which can have multiple midribs. The Trf mutation is located in the DNA-binding domain of ZmARF28, a member of the repressive class-B Auxin Response Factor clade that we know relatively little about. Our unique comparative analysis of maize and moss, species separated by ~500 million years of evolution, reveals a novel evolutionarily conserved degradation region, shedding light on a new pathway for class-B ARF regulation in plants. Through investigating Ojaand Trf we not only build new understanding of auxin-regulated development in maize, but also uncover fundamental components of auxin response regulation important for land plants.
@drannisr.bsky.social
https://www.linkedin.com/in/annis-richardson-4b89965b www.theplantshapelab.org
15th June 2026: Zoe Nahas (University of Lausanne, Switzerland) & Toby Andrews (Institute of Developmental and Regenerative Medicine, University of Oxford, UK)
Location: online on Zoom
Zoe Nahas:Regulation of shoot branching in plants: competition between modular parts
Plants achieve extraordinary flexibility of form through their modular growth, allowing their body plan to adapt to the prevailing environmental conditions. Above ground, plants continuously tune their shoot architecture by regulating the growth of axillary buds, which are derived from meristems established in the axil of each leaf. Each meristem either stays dormant as a bud or grows into a branch that has the same developmental potential as the main stem. The decision for a bud to grow out depends on the integration of local signals in the bud and systemic signals from across the plant, such as the activity of other branches on the same plant. This occurs via at least two well-established hubs, with local bud regulation via the transcription factor BRANCHED1, and systemic regulation via the transport network of the plant hormone auxin, although the interplay between these two hubs is poorly understood. We investigated this interplay in the context of competition between buds. We combined experiments with a simple mathematical model that represents two buds as a self-activating and mutually-inhibiting system. When representing BRANCHED1 as modulating the competitive strength of each bud, our model recapitulates a range of experimental data and makes testable predictions which we largely validate. Overall, this work develops an integrated model of shoot branching regulation that accounts for the ability of plants to adjust dynamically both the number and location of growing branches.
TobyAndrews: Adaptive morphogenesis at the heart-blood interface
From a single fertilized egg, embryonic cells sculpt organs with intricate physical architectures that confer essential functions. While mechanical and biochemical cues tightly control cell behaviours in the embryo, organ shape, size and function are remarkably sensitive to fluctuations in the developmental environment, leading to adaptive and pathological changes in form. Our goal is to understand how environmental cues interact with intrinsic developmental programmes to produce structural diversity across populations and species, and devise mechanisms to restore normal organ function when development goes awry.
In the developing heart, remodelling of the myocardial wall produces a porous trabecular meshwork that invades into the ventricle lumen and into the paths of circulating blood cells. This increases the efficiency of heart contraction, and expands the surface area for myocardial gas exchange. Here, using CRISPR-Cas9 to produce modular anaemic phenotypes, we show that the dynamics of trabecular growth are tightly regulated by the efficiency of oxygen delivery by circulating red blood cells. Specifically, experimental disruption of haemoglobin production leads to accelerated trabecular growth, and an expanded surface area of contact with the blood. To test the intrinsic oxygen sensitivity of the myocardium, we generated new transgenic lines with pseudo-hypoxic and hypoxia-resistant myocardia. While hypoxia-resistant myocardia exhibit severely delayed trabeculation, pseudo-hypoxic myocardia produce multicellular trabecular ridges 48 hours early, leading to rapid occlusion of the ventricle lumen and cessation of blood flow. In parallel, tracking of single red blood cells using mosaic fluorescent labelling and lightfield microscopy shows that trabecular growth both slows intracardiac blood flow and traps a fraction of red blood cells within its lattice structure. Together, these findings hint at a dynamic adaptive mechanism, in which early hypoxia in the myocardium initiates a morphogenetic programme that stalls blood flow, thereby improving oxygen extraction from circulating blood cells. Ongoing work is investigating how inappropriate activation of these mechanisms contributes to the aetiology of congenital birth defects, and has supported the evolutionary radiation of aquatic species into environmental extremes.
