@article{21383,
abstract = {Planarian flatworms are known for their remarkable regenerative capacity; however, the precise intercellular communication mechanisms underlying this process remain unsolved. Here, we report the discovery and characterization of abundant extracellular vesicles (EVs) in planarians. Using imaging and molecular analysis, we show conservation of biogenesis, morphology, and protein composition of planarian EVs. Environmental stressors significantly elevate EV release, indicating that planarians dynamically regulate vesicle production. Functionally, planarian EVs mediate intercellular communication by transferring regulatory signals: We find that they shuttle small RNAs that effect systemic RNA interference (RNAi) throughout the organism. Notably, gene knockdown experiments reveal a crucial role for AGO-3, a member of the Argonaute family of proteins, in modulating the association of small interfering RNAs with EVs, linking the intracellular RNAi machinery to EV-based signaling. These findings highlight EVs as pivotal mediators of cell-cell communication in planarians, with broad implications for understanding the coordination of gene regulation and tissue regeneration in animals.},
author = {Sasidharan, Vidyanand and Ancellotti, Laura and Doddihal, Viraj and Brewster, Carolyn and Mann, Frederick and McKinney, Mary Cathleen and Varberg, Joseph and Ross, Eric and Deng, Fengyan and Yi, Kexi and Sánchez Alvarado, Alejandro},
issn = {2375-2548},
journal = {Science Advances},
number = {6},
publisher = {American Association for the Advancement of Science},
title = {{Extracellular vesicles mediate stem cell signaling and systemic RNAi in planarians}},
doi = {10.1126/sciadv.ady1461},
volume = {12},
year = {2026},
}
@misc{21137,
author = {Naik, Suyash},
publisher = {Institute of Science and Technology Austria},
title = {{Data associated with Keratins coordinate tissue spreading }},
doi = {10.15479/AT-ISTA-21137},
year = {2026},
}
@article{21015,
abstract = {Early embryo geometry is one of the most invariant species-specific traits, yet its role in ensuring developmental reproducibility and robustness remains underexplored. Here we show that in zebrafish, the geometry of the fertilized egg—specifically its curvature and volume—serves as a critical initial condition triggering a cascade of events that influence development. The embryo geometry guides patterned asymmetric cell divisions in the blastoderm, generating radial gradients of cell volume and nucleocytoplasmic ratio. These gradients generate mitotic phase waves, with the nucleocytoplasmic ratio determining individual cell cycle periods independently of other cells. We demonstrate that reducing cell autonomy reshapes these waves, emphasizing the instructive role of geometry-derived volume patterns in setting the intrinsic period of the cell cycle oscillator. In addition to organizing cell cycles, early embryo geometry spatially patterns zygotic genome activation at the midblastula transition, a key step in establishing embryonic autonomy. Disrupting the embryo shape alters the zygotic genome activation pattern and causes ectopic germ layer specification, underscoring the developmental significance of geometry. Together, our findings reveal a symmetry-breaking function of early embryo geometry in coordinating cell cycle and transcriptional patterning.},
author = {Mishra, Nikhil and Li, Yuting I and Hannezo, Edouard B and Heisenberg, Carl-Philipp J},
issn = {1745-2481},
journal = {Nature Physics},
pages = {139--150},
publisher = {Springer Nature},
title = {{Geometry-driven asymmetric cell divisions pattern cell cycles and zygotic genome activation in the zebrafish embryo}},
doi = {10.1038/s41567-025-03122-1},
volume = {22},
year = {2026},
}
@article{20048,
abstract = {During embryonic development, cell behaviors need to be tightly regulated in time and space. Yet how the temporal and spatial regulations of cell behaviors are interconnected during embryonic development remains elusive. To address this, we turned to zebrafish gastrulation, the process whereby dynamic cell behaviors generate the three principal germ layers of the early embryo. Here, we show that Hoxb cluster genes are expressed in a temporally collinear manner at the blastoderm margin, where mesodermal and endodermal (mesendoderm) progenitor cells are specified and ingress to form mesendoderm/hypoblast. Functional analysis shows that these Hoxb genes regulate the timing of cell ingression: under- or overexpression of Hoxb genes perturb the timing of mesendoderm cell ingression and, consequently, the positioning of these cells along the forming anterior-posterior body axis after gastrulation. Finally, we found that Hoxb genes control the timing of mesendoderm ingression by regulating cellular bleb formation and cell surface fluctuations in the ingressing cells. Collectively, our findings suggest that Hoxb genes interconnect the temporal and spatial pattern of cell behaviors during zebrafish gastrulation by controlling cell surface fluctuations.},
author = {Moriyama, Yuuta and Mitsui, Toshiyuki and Heisenberg, Carl-Philipp J},
issn = {1477-9129},
journal = {Development},
number = {12},
publisher = {The Company of Biologists},
title = {{Hoxb genes determine the timing of cell ingression by regulating cell surface fluctuations during zebrafish gastrulation}},
doi = {10.1242/dev.204261},
volume = {152},
year = {2025},
}
@article{20183,
abstract = {The unequal segregation of organelles has been proposed to be an intrinsic mechanism that contributes to cell fate divergence during asymmetric cell division; however, in vivo evidence is sparse. Using super-resolution microscopy, we analysed the segregation of organelles during the division of the neuroblast QL.p in C. elegans larvae. QL.p divides to generate a daughter that survives, QL.pa, and a daughter that dies, QL.pp. We found that mitochondria segregate unequally by density and morphology and that this is dependent on mitochondrial dynamics. Furthermore, we found that mitochondrial density in QL.pp correlates with the time it takes QL.pp to die. We propose that low mitochondrial density in QL.pp promotes the cell death fate and ensures that QL.pp dies in a highly reproducible and timely manner. Our results provide in vivo evidence that the unequal segregation of mitochondria can contribute to cell fate divergence during asymmetric cell division in a developing animal.},
author = {Segos, Ioannis and Van Eeckhoven, Jens and Berger, Simon and Mishra, Nikhil and Lambie, Eric J. and Conradt, Barbara},
issn = {2041-1723},
journal = {Nature Communications},
publisher = {Springer Nature},
title = {{Unequal segregation of mitochondria during asymmetric cell division contributes to cell fate divergence in sister cells in vivo}},
doi = {10.1038/s41467-025-62484-5},
volume = {16},
year = {2025},
}
@article{20188,
abstract = {Collective cell migration is coordinated by the front-to-rear intercellular propagation of EGFR-Ras-ERK pathway activation. However, the molecular mechanisms integrating front-to-rear information into this intercellular signaling cascade, particularly the determinants of cellular front-side specification, remain elusive. We visualized the activity of EGFR, Ras, Rac1 and Rab5A (hereafter Rab5) by using FRET biosensors and chemogenetic tools. Whereas EGFR activation was uniformly observed within cells, Ras activation was biased to the front side within cells. The polarized Ras activation depended on Merlin and Rac1, which also showed front-biased activation. Furthermore, Rab5, a crucial regulator of cell migration, demonstrated similar front-biased activation and was found to function downstream of Ras while being necessary for Rac1 activation. Thus, the positive feedback loop consisting of Ras, Rab5 and Rac1 is activated primarily at the front of collectively migrating cells. These findings offer new spatio-temporal insight into processing front–rear information during collective cell migration.},
author = {Jikko, Yuya and Deguchi, Eriko and Matsuda, Kimiya and Hino, Naoya and Tsukiji, Shinya and Matsuda, Michiyuki and Terai, Kenta},
issn = {1477-9137},
journal = {Journal of Cell Science},
number = {15},
publisher = {The Company of Biologists},
title = {{Front-biased activation of the Ras-Rab5-Rac1 loop coordinates collective cell migration}},
doi = {10.1242/jcs.263779},
volume = {138},
year = {2025},
}
@article{20349,
abstract = {Oogenesis – the formation and development of an oocyte – is fundamental to reproduction and embryonic development. Due to its accessibility to genetic manipulations and the ability to culture and experimentally manipulate oocytes ex vivo, zebrafish has emerged as a powerful vertebrate model system for studying oogenesis. In this review, we provide a comprehensive overview of zebrafish oogenesis, from early germ cell formation to oocyte maturation and fertilization. We discuss recent advances in uncovering the molecular and cellular mechanisms driving this complex process and highlight key knowledge gaps that remain to be addressed.},
author = {Hofmann, Laura and Heisenberg, Carl-Philipp J},
issn = {1096-3634},
journal = {Seminars in Cell and Developmental Biology},
publisher = {Elsevier},
title = {{Decoding zebrafish oogenesis: From primordial germ cell development to fertilization}},
doi = {10.1016/j.semcdb.2025.103650},
volume = {175},
year = {2025},
}
@article{19404,
abstract = {Cell migration is a fundamental process during embryonic development. Most studies in vivo have focused on the migration of cells using the extracellular matrix (ECM) as their substrate for migration. In contrast, much less is known about how cells migrate on other cells, as found in early embryos when the ECM has not yet formed. Here, we show that lateral mesendoderm (LME) cells in the early zebrafish gastrula use the ectoderm as their substrate for migration. We show that the lateral ectoderm is permissive for the animal-pole-directed migration of LME cells, while the ectoderm at the animal pole halts it. These differences in permissiveness depend on the lateral ectoderm being more cohesive than the animal ectoderm, a property controlled by bone morphogenetic protein (BMP) signaling within the ectoderm. Collectively, these findings identify ectoderm tissue cohesion as one critical factor in regulating LME migration during zebrafish gastrulation.},
author = {Tavano, Ste and Brückner, David and Tasciyan, Saren and Tong, Xin and Kardos, Roland and Schauer, Alexandra and Hauschild, Robert and Heisenberg, Carl-Philipp J},
issn = {2211-1247},
journal = {Cell Reports},
number = {3},
publisher = {Elsevier},
title = {{BMP-dependent patterning of ectoderm tissue material properties modulates lateral mesendoderm cell migration during early zebrafish gastrulation}},
doi = {10.1016/j.celrep.2025.115387},
volume = {44},
year = {2025},
}
@phdthesis{20441,
abstract = {Epithelial spreading plays a pivotal role in the development of organisms especially those
such as zebrafish which require the epithelial enveloping layer (EVL) to spread to cover the
substantial yolk surface during gastrulation. Epiboly requires the transition of the epithelium
with cuboidal cells to form a thin, flat squamous epithelial sheet. During this transition, the
cells show tissue-scale mechanosensation with mechanisms such as direct mechanical control
over the axis of cell division.
Cytoskeletal intermediate filaments play a crucial role in vertebrate cells, not only facilitating
mechanical stability but also helping facilitate the mechanosensitive response of the cell.
Mechanosenstivity displayed by intermediate filaments is due not just to their interesting
physical properties but also to their interactions with other cytoskeletal elements such as actin
and microtubules. Keratin is the predominant intermediate filament expressed in the EVL.
It expresses concomitantly with the gastrulation movements of the developing embryo. Our
work focuses on understanding the role and dynamics of the keratin cytoskeletal network in
modulating the physical aspects of EVL spreading. We demonstrated with the combination of
physical characterisation and manipulations of the EVL, utilising a variety of biophysical tools
and microscopy, the mechanistic role of keratin in tissue spreading.
Generating novel genetic morphants and mutants, we probe the effect that the loss of the
keratin network has on the physiology of the epithelium and the developing embryo. We
show that the changing organisation of the keratin network is important for changing EVL
physical properties as the stress imposed on the EVL increases during epiboly. By modelling
the epithelium, we study how the mechanical heterogeneity in an epithelium can feed back into
a mechanical loop to the maturation of the keratin network and hence affect the mechanics
of the epithelium. However, unlike what would be predicted by the effect of intermediate
filaments in acting as a security belt and increasing the resistance of the epithelium, we observe
that loss of keratin leads to a delay in the EVL movement. Using both local aspirations of the
YSL and EVL ablations, we demonstrate the mechanistic facilitation of actin mechanosensation
in a keratin-dependent manner.
Furthermore, using chemical inhibitors of microtubule polymerisation, we provide insight into
the mechanisms underlying the organisation and distribution of keratin. Interestingly, the
phenotype observed upon this loss of microtubules shows that keratins interact with the nucleus
through microtubular interactions. Together with these diverse observations, we describe
the mechanosensory feedback between resilience and that is critical for uniform and robust
spreading of the epithelium.},
author = {Naik, Suyash},
isbn = {978-3-99078-069-5},
issn = {2663-337X},
pages = {105},
publisher = {Institute of Science and Technology Austria},
title = {{Keratins act as global coordinators of tissue spreading through mechanosensitive feedback}},
doi = {10.15479/AT-ISTA-20441},
year = {2025},
}
@unpublished{20465,
abstract = {For tissues to spread, they must be deformable while maintaining their structural integrity. How these opposing requirements are balanced within spreading tissues is not yet well understood. Here, we show that keratin intermediate filaments function in epithelial spreading by adapting tissue mechanical resilience to the stresses arising in the tissue during the spreading process. By analysing the expansion of the enveloping cell layer (EVL) over the large yolk cell in early zebrafish embryos in vivo, we found that keratin network maturation in EVL cells is promoted by stresses building up within the spreading tissue. Through genetic interference and tissue rheology experiments, complemented by a vertex model with mechanochemical feedback, we demonstrate that stress-induced keratin network maturation in the EVL increases tissue viscosity, which is essential for preventing tissue rupture. Interestingly, keratins are also required in the yolk cell for mechanosensitive actomyosin network contraction and flow, the force-generating processes pulling the EVL. These dual mechanosensitive functions of keratins enable a balance between pulling force production in the yolk cell and the mechanical resilience of the EVL against stresses generated by these pulling forces, thereby ensuring uniform and robust tissue spreading.},
author = {Naik, Suyash and Keta, Yann-Edwin and Pranjic-Ferscha, Kornelija and Hannezo, Edouard B and Henkes, Silke and Heisenberg, Carl-Philipp J},
booktitle = {bioRxiv},
publisher = {Cold Spring Harbor Laboratory},
title = {{Keratins coordinate tissue spreading by balancing spreading forces with tissue material properties}},
doi = {10.1101/2025.02.14.638262},
year = {2025},
}
@article{18651,
abstract = {Embryo axis formation begins with the localized expression of biochemical signals, which organize cell movements and determine cell fate. A quail study finds that tissue contraction and resulting long-range changes in tissue tension restrict the area where these biochemical signals are expressed.},
author = {Hino, Naoya and Santos Fernandes Lasbarrères Camelo, Carolina and Heisenberg, Carl-Philipp J},
issn = {1879-0445},
journal = {Current Biology},
number = {24},
pages = {R1230--R1232},
publisher = {Elsevier},
title = {{Development: Turing mechanics}},
doi = {10.1016/j.cub.2024.10.065},
volume = {34},
year = {2024},
}
@article{18940,
abstract = {BMP signaling has a conserved function in patterning the dorsal-ventral body axis in Bilateria and the directive axis in anthozoan cnidarians. So far, cnidarian studies have focused on the role of different BMP signaling network components in regulating pSMAD1/5 gradient formation. Much less is known about the target genes downstream of BMP signaling. To address this, we generated a genome-wide list of direct pSMAD1/5 target genes in the anthozoan Nematostella vectensis, several of which were conserved in Drosophila and Xenopus. Our ChIP-seq analysis revealed that many of the regulatory molecules with documented bilaterally symmetric expression in Nematostella are directly controlled by BMP signaling. We identified several so far uncharacterized BMP-dependent transcription factors and signaling molecules, whose bilaterally symmetric expression may be indicative of their involvement in secondary axis patterning. One of these molecules is zswim4-6, which encodes a novel nuclear protein that can modulate the pSMAD1/5 gradient and potentially promote BMP-dependent gene repression.},
author = {Knabl, Paul and Schauer, Alexandra and Pomreinke, Autumn P and Zimmermann, Bob and Rogers, Katherine W and Čapek, Daniel and Müller, Patrick and Genikhovich, Grigory},
issn = {2050-084X},
journal = {eLife},
publisher = {eLife Sciences Publications},
title = {{Analysis of SMAD1/5 target genes in a sea anemone reveals ZSWIM4-6 as a novel BMP signaling modulator}},
doi = {10.7554/elife.80803},
volume = {13},
year = {2024},
}
@article{14795,
abstract = {Metazoan development relies on the formation and remodeling of cell-cell contacts. Dynamic reorganization of adhesion receptors and the actomyosin cell cortex in space and time plays a central role in cell-cell contact formation and maturation. Nevertheless, how this process is mechanistically achieved when new contacts are formed remains unclear. Here, by building a biomimetic assay composed of progenitor cells adhering to supported lipid bilayers functionalized with E-cadherin ectodomains, we show that cortical F-actin flows, driven by the depletion of myosin-2 at the cell contact center, mediate the dynamic reorganization of adhesion receptors and cell cortex at the contact. E-cadherin-dependent downregulation of the small GTPase RhoA at the forming contact leads to both a depletion of myosin-2 and a decrease of F-actin at the contact center. At the contact rim, in contrast, myosin-2 becomes enriched by the retraction of bleb-like protrusions, resulting in a cortical tension gradient from the contact rim to its center. This tension gradient, in turn, triggers centrifugal F-actin flows, leading to further accumulation of F-actin at the contact rim and the progressive redistribution of E-cadherin from the contact center to the rim. Eventually, this combination of actomyosin downregulation and flows at the contact determines the characteristic molecular organization, with E-cadherin and F-actin accumulating at the contact rim, where they are needed to mechanically link the contractile cortices of the adhering cells.},
author = {Arslan, Feyza N and Hannezo, Edouard B and Merrin, Jack and Loose, Martin and Heisenberg, Carl-Philipp J},
issn = {1879-0445},
journal = {Current Biology},
number = {1},
pages = {171--182.e8},
publisher = {Elsevier},
title = {{Adhesion-induced cortical flows pattern E-cadherin-mediated cell contacts}},
doi = {10.1016/j.cub.2023.11.067},
volume = {34},
year = {2024},
}
@article{14846,
abstract = {Contraction and flow of the actin cell cortex have emerged as a common principle by which cells reorganize their cytoplasm and take shape. However, how these cortical flows interact with adjacent cytoplasmic components, changing their form and localization, and how this affects cytoplasmic organization and cell shape remains unclear. Here we show that in ascidian oocytes, the cooperative activities of cortical actomyosin flows and deformation of the adjacent mitochondria-rich myoplasm drive oocyte cytoplasmic reorganization and shape changes following fertilization. We show that vegetal-directed cortical actomyosin flows, established upon oocyte fertilization, lead to both the accumulation of cortical actin at the vegetal pole of the zygote and compression and local buckling of the adjacent elastic solid-like myoplasm layer due to friction forces generated at their interface. Once cortical flows have ceased, the multiple myoplasm buckles resolve into one larger buckle, which again drives the formation of the contraction pole—a protuberance of the zygote’s vegetal pole where maternal mRNAs accumulate. Thus, our findings reveal a mechanism where cortical actomyosin network flows determine cytoplasmic reorganization and cell shape by deforming adjacent cytoplasmic components through friction forces.},
author = {Caballero Mancebo, Silvia and Shinde, Rushikesh and Bolger-Munro, Madison and Peruzzo, Matilda and Szep, Gregory and Steccari, Irene and Labrousse Arias, David and Zheden, Vanessa and Merrin, Jack and Callan-Jones, Andrew and Voituriez, Raphaël and Heisenberg, Carl-Philipp J},
issn = {1745-2481},
journal = {Nature Physics},
pages = {310--321},
publisher = {Springer Nature},
title = {{Friction forces determine cytoplasmic reorganization and shape changes of ascidian oocytes upon fertilization}},
doi = {10.1038/s41567-023-02302-1},
volume = {20},
year = {2024},
}
@article{15048,
abstract = {Embryogenesis results from the coordinated activities of different signaling pathways controlling cell fate specification and morphogenesis. In vertebrate gastrulation, both Nodal and BMP signaling play key roles in germ layer specification and morphogenesis, yet their interplay to coordinate embryo patterning with morphogenesis is still insufficiently understood. Here, we took a reductionist approach using zebrafish embryonic explants to study the coordination of Nodal and BMP signaling for embryo patterning and morphogenesis. We show that Nodal signaling triggers explant elongation by inducing mesendodermal progenitors but also suppressing BMP signaling activity at the site of mesendoderm induction. Consistent with this, ectopic BMP signaling in the mesendoderm blocks cell alignment and oriented mesendoderm intercalations, key processes during explant elongation. Translating these ex vivo observations to the intact embryo showed that, similar to explants, Nodal signaling suppresses the effect of BMP signaling on cell intercalations in the dorsal domain, thus allowing robust embryonic axis elongation. These findings suggest a dual function of Nodal signaling in embryonic axis elongation by both inducing mesendoderm and suppressing BMP effects in the dorsal portion of the mesendoderm.},
author = {Schauer, Alexandra and Pranjic-Ferscha, Kornelija and Hauschild, Robert and Heisenberg, Carl-Philipp J},
issn = {1477-9129},
journal = {Development},
number = {4},
pages = {1--18},
publisher = {The Company of Biologists},
title = {{Robust axis elongation by Nodal-dependent restriction of BMP signaling}},
doi = {10.1242/dev.202316},
volume = {151},
year = {2024},
}
@article{15301,
abstract = {Plant morphogenesis relies exclusively on oriented cell expansion and division. Nonetheless, the mechanism(s) determining division plane orientation remain elusive. Here, we studied tissue healing after laser-assisted wounding in roots of Arabidopsis thaliana and uncovered how mechanical forces stabilize and reorient the microtubule cytoskeleton for the orientation of cell division. We identified that root tissue functions as an interconnected cell matrix, with a radial gradient of tissue extendibility causing predictable tissue deformation after wounding. This deformation causes instant redirection of expansion in the surrounding cells and reorientation of microtubule arrays, ultimately predicting cell division orientation. Microtubules are destabilized under low tension, whereas stretching of cells, either through wounding or external aspiration, immediately induces their polymerization. The higher microtubule abundance in the stretched cell parts leads to the reorientation of microtubule arrays and, ultimately, informs cell division planes. This provides a long-sought mechanism for flexible re-arrangement of cell divisions by mechanical forces for tissue reconstruction and plant architecture.},
author = {Hörmayer, Lukas and Montesinos López, Juan C and Trozzi, N and Spona, Leonhard and Yoshida, Saiko and Marhavá, Petra and Caballero Mancebo, Silvia and Benková, Eva and Heisenberg, Carl-Philipp J and Dagdas, Y and Majda, M and Friml, Jiří},
issn = {1878-1551},
journal = {Developmental Cell},
number = {10},
pages = {1333--1344.e4},
publisher = {Elsevier},
title = {{Mechanical forces in plant tissue matrix orient cell divisions via microtubule stabilization}},
doi = {10.1016/j.devcel.2024.03.009},
volume = {59},
year = {2024},
}
@article{14041,
abstract = {Tissue morphogenesis and patterning during development involve the segregation of cell types. Segregation is driven by differential tissue surface tensions generated by cell types through controlling cell-cell contact formation by regulating adhesion and actomyosin contractility-based cellular cortical tensions. We use vertebrate tissue cell types and zebrafish germ layer progenitors as in vitro models of 3-dimensional heterotypic segregation and developed a quantitative analysis of their dynamics based on 3D time-lapse microscopy. We show that general inhibition of actomyosin contractility by the Rho kinase inhibitor Y27632 delays segregation. Cell type-specific inhibition of non-muscle myosin2 activity by overexpression of myosin assembly inhibitor S100A4 reduces tissue surface tension, manifested in decreased compaction during aggregation and inverted geometry observed during segregation. The same is observed when we express a constitutively active Rho kinase isoform to ubiquitously keep actomyosin contractility high at cell-cell and cell-medium interfaces and thus overriding the interface-specific regulation of cortical tensions. Tissue surface tension regulation can become an effective tool in tissue engineering.},
author = {Méhes, Elod and Mones, Enys and Varga, Máté and Zsigmond, Áron and Biri-Kovács, Beáta and Nyitray, László and Barone, Vanessa and Krens, Gabriel and Heisenberg, Carl-Philipp J and Vicsek, Tamás},
issn = {2399-3642},
journal = {Communications Biology},
publisher = {Springer Nature},
title = {{3D cell segregation geometry and dynamics are governed by tissue surface tension regulation}},
doi = {10.1038/s42003-023-05181-7},
volume = {6},
year = {2023},
}
@article{14080,
abstract = {Extracellular signal-regulated kinase (ERK) has been recognized as a critical regulator in various physiological and pathological processes. Extensive research has elucidated the signaling mechanisms governing ERK activation via biochemical regulations with upstream molecules, particularly receptor tyrosine kinases (RTKs). However, recent advances have highlighted the role of mechanical forces in activating the RTK–ERK signaling pathways, thereby opening new avenues of research into mechanochemical interplay in multicellular tissues. Here, we review the force-induced ERK activation in cells and propose possible mechanosensing mechanisms underlying the mechanoresponsive ERK activation. We conclude that mechanical forces are not merely passive factors shaping cells and tissues but also active regulators of cellular signaling pathways controlling collective cell behaviors.},
author = {Hirashima, Tsuyoshi and Hino, Naoya and Aoki, Kazuhiro and Matsuda, Michiyuki},
issn = {1879-0410},
journal = {Current Opinion in Cell Biology},
number = {10},
publisher = {Elsevier},
title = {{Stretching the limits of extracellular signal-related kinase (ERK) signaling — Cell mechanosensing to ERK activation}},
doi = {10.1016/j.ceb.2023.102217},
volume = {84},
year = {2023},
}
@article{14082,
abstract = {Epithelial barrier function is commonly analyzed using transepithelial electrical resistance, which measures ion flux across a monolayer, or by adding traceable macromolecules and monitoring their passage across the monolayer. Although these methods measure changes in global barrier function, they lack the sensitivity needed to detect local or transient barrier breaches, and they do not reveal the location of barrier leaks. Therefore, we previously developed a method that we named the zinc-based ultrasensitive microscopic barrier assay (ZnUMBA), which overcomes these limitations, allowing for detection of local tight junction leaks with high spatiotemporal resolution. Here, we present expanded applications for ZnUMBA. ZnUMBA can be used in Xenopus embryos to measure the dynamics of barrier restoration and actin accumulation following laser injury. ZnUMBA can also be effectively utilized in developing zebrafish embryos as well as cultured monolayers of Madin–Darby canine kidney (MDCK) II epithelial cells. ZnUMBA is a powerful and flexible method that, with minimal optimization, can be applied to multiple systems to measure dynamic changes in barrier function with spatiotemporal precision.},
author = {Higashi, Tomohito and Stephenson, Rachel E. and Schwayer, Cornelia and Huljev, Karla and Higashi, Atsuko Y. and Heisenberg, Carl-Philipp J and Chiba, Hideki and Miller, Ann L.},
issn = {1477-9137},
journal = {Journal of Cell Science},
number = {15},
publisher = {The Company of Biologists},
title = {{ZnUMBA - a live imaging method to detect local barrier breaches}},
doi = {10.1242/jcs.260668},
volume = {136},
year = {2023},
}
@article{12830,
abstract = {Interstitial fluid (IF) accumulation between embryonic cells is thought to be important for embryo patterning and morphogenesis. Here, we identify a positive mechanical feedback loop between cell migration and IF relocalization and find that it promotes embryonic axis formation during zebrafish gastrulation. We show that anterior axial mesendoderm (prechordal plate [ppl]) cells, moving in between the yolk cell and deep cell tissue to extend the embryonic axis, compress the overlying deep cell layer, thereby causing IF to flow from the deep cell layer to the boundary between the yolk cell and the deep cell layer, directly ahead of the advancing ppl. This IF relocalization, in turn, facilitates ppl cell protrusion formation and migration by opening up the space into which the ppl moves and, thereby, the ability of the ppl to trigger IF relocalization by pushing against the overlying deep cell layer. Thus, embryonic axis formation relies on a hydraulic feedback loop between cell migration and IF relocalization.},
author = {Huljev, Karla and Shamipour, Shayan and Nunes Pinheiro, Diana C and Preusser, Friedrich and Steccari, Irene and Sommer, Christoph M and Naik, Suyash and Heisenberg, Carl-Philipp J},
issn = {1878-1551},
journal = {Developmental Cell},
number = {7},
pages = {582--596.e7},
publisher = {Elsevier},
title = {{A hydraulic feedback loop between mesendoderm cell migration and interstitial fluid relocalization promotes embryonic axis formation in zebrafish}},
doi = {10.1016/j.devcel.2023.02.016},
volume = {58},
year = {2023},
}