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Jifeng Liu, Anne Grapin-Botton
Benchmarking in vivo and in vitro gene co-expression networks enables efficient β-like cell differentiation.
Dev Cell, 61(2) 229-231 (2026)
PubMed Source   

In this issue of Developmental Cell, Yu et al.1 reconstruct human embryonic gene co-expression networks (GCNs) that guide pancreatic endocrine lineage specification. Benchmarking stem cell-derived islet (SC-islet) differentiation protocols against fetal human pancreatic cells reveals early regulatory divergences, thereby enabling the design of a protocol with improved β-like cell production.
@article{Liu9146,
author={Jifeng Liu, Anne Grapin-Botton},
title={Benchmarking in vivo and in vitro gene co-expression networks enables efficient β-like cell differentiation.},
journal ={Developmental cell},
volume={61},
issue ={2},
pages={229--231},
year=2026
}

Vasco Köhling, Florian Peters, Inez Götting, Emil Fries, Niklas Beck, Fred Armbrust, Silje Beckinger, Cynthia Bülck, Vahap Canbay, Inken Harder, Marion Mengel, Malina Rüffer, Kira Bickenbach, Konstantinos Kalogeropoulos, Michaela Schweizer, Marian Lewerenz, Neele Schumacher, Nathalie Jonca, Michael Haase, Ronald Naumann, Ulrich Auf dem Keller, Christoph Becker-Pauly, Sascha Rüffer
Regulation of keratinocyte proliferation and epidermal inflammation by meprin α-mediated cleavage of dermokine.
J Invest Dermatol, Art. No. doi: 10.1016/j.jid.2026.01.034 (2026)
PubMed Source   

Dysregulations within the epidermal proteolytic network can cause hyperproliferative and inflammatory disorders. While the metalloprotease meprin α is localized in the stratum basale in healthy skin, increased levels are found in the upper epidermal layers in wound healing and psoriatic lesions. To investigate a link between meprin α expression and keratinocyte proliferation, we developed a mouse model for inducible expression of pathological meprin α levels (K5Mα). K5Mα mice developed a skin phenotype characterized by hyperkeratosis, acanthosis, parakeratosis and barrier defect. Keratinocyte hyperproliferation and local inflammation were induced upon induction of meprin α expression. By N-terminomics we identified dermokine, a regulator of keratinocyte proliferation and epidermal immune response, as a putative substrate of meprin α. We validated the proteolysis and identified the cleavage site, which is highly conserved in mammals, suggesting that dermokine degradation by meprin α represents a central mechanism in wound healing and hyperproliferative skin diseases.
@article{Köhling9145,
author={Vasco Köhling, Florian Peters, Inez Götting, Emil Fries, Niklas Beck, Fred Armbrust, Silje Beckinger, Cynthia Bülck, Vahap Canbay, Inken Harder, Marion Mengel, Malina Rüffer, Kira Bickenbach, Konstantinos Kalogeropoulos, Michaela Schweizer, Marian Lewerenz, Neele Schumacher, Nathalie Jonca, Michael Haase, Ronald Naumann, Ulrich Auf dem Keller, Christoph Becker-Pauly, Sascha Rüffer},
title={Regulation of keratinocyte proliferation and epidermal inflammation by meprin α-mediated cleavage of dermokine.},
journal ={The Journal of investigative dermatology},
volume={},
pages={1--1},
year=2026
}

Alun R C Jones, Alina A Mikhailova, Cédric Aumont, Juliette Berger, Cong Liu, Shulin He, Zongqing Wang, Sylke Winkler, Erich Bornberg-Bauer, Frédéric Legendre#, Dino P McMahon#, Mark C Harrison#
Cryptocercus genomes expand knowledge of adaptations to xylophagy and termite sociality.
Genome Biol Evol, Art. No. doi: 10.1093/gbe/evag028 (2026)
Open Access PubMed Source   

Subsociality and wood-eating or xylophagy are understood as key drivers in the evolution of eusociality in Blattodea (cockroaches and termites), two features observed in the cockroach genus Cryptocercus, the sister group of all termites. We analyse two high-quality genomes from this genus, C. punctulatus from North America and C. meridianus from Southeast Asia, to explore the evolutionary transitions to xylophagy and subsociality within Blattodea. Our analyses reveal evidence of relaxed selection in both Cryptocercus and termites, indicating that a reduction in effective population size may have occurred in their subsocial ancestors. These findings challenge the expected positive correlation between dN/dS ratios and social complexity, as Cryptocercus exhibits elevated dN/dS values that may exceed those of eusocial termites. Additionally, we infer a reduction in the number of Ionotropic Receptors and a change from uni- to bimodal methylation signatures in protein coding genes in a common ancestor of Cryptocercus and termites, mechanisms previously thought to have evolved with the emergence of eusociality in termites. Future studies incorporating additional genomic data from diverse blattodean species can further build on these findings and provide deeper insights into the molecular mechanisms driving transitions to xylophagy and eusociality.
@article{Jones9143,
author={Alun R C Jones, Alina A Mikhailova, Cédric Aumont, Juliette Berger, Cong Liu, Shulin He, Zongqing Wang, Sylke Winkler, Erich Bornberg-Bauer, Frédéric Legendre, Dino P McMahon, Mark C Harrison},
title={Cryptocercus genomes expand knowledge of adaptations to xylophagy and termite sociality.},
journal ={Genome biology and evolution},
volume={},
pages={1--1},
year=2026
}

Jinghui Liu*, Elisa Nerli*, Charlie Duclut, Amit S Vishen, Naomi Berbee, Sylvia Kaufmann, Cesar Ponce, Aristides B. Arrenberg, Frank Jülicher#, Rita Mateus#
Injury-induced electrochemical coupling triggers organ growth.
Sci Adv, 12(6) Art. No. 687 (2026)
Open Access PubMed Source   

Organ injury triggers nonneuronal electric currents essential for regeneration. However, the mechanisms by which electrical signals are generated, sensed, and transmitted upon damage to promote organ growth remain unclear. Here, we uncover that organ repair relies on dynamic electrochemical coupling between membrane potential depolarization and intracellular signaling, essential to activate cell proliferation. By subsecond live imaging of locally injured zebrafish larval fins, we identify events across time and space: a millisecond, long-range, membrane depolarization gradient, followed by second-persistent intracellular calcium responses. In the subsequent hour, voltage sensing phosphatase senses the injury-driven membrane potential change and autonomously translates the electric signal intracellularly, promoting tissue-wide cell proliferation. Connecting these dynamics with an electrodiffusive model showed that ionic fluxes and electric potential become coupled in the fin's interstitial space, enabling organ-wide signal spreading. Our work reveals the coupling between fast electrical signals and slower intracellular signaling, ensuring complete organ recovery.
@article{Liu9135,
author={Jinghui Liu, Elisa Nerli, Charlie Duclut, Amit S Vishen, Naomi Berbee, Sylvia Kaufmann, Cesar Ponce, Aristides B. Arrenberg, Frank Jülicher, Rita Mateus},
title={Injury-induced electrochemical coupling triggers organ growth.},
journal ={Science advances},
volume={12},
issue ={6},
pages={null--null},
year=2026
}

Rashmiparvathi Keshara, Karolina Kuodyte, Antje Janosch, Cordula Andree, Marc Bickle, Martin Stöter, Rico Barsacchi, Yung Hae Kim, Anne Grapin-Botton
High-content screening of organoids reveals the mechanisms of human pancreas acinar specification.
Cell Stem Cell, 33(2) 325-339 (2026)
Open Access PubMed Source   

Organoids derived from pluripotent stem cells have emerged as powerful models to study human development. To investigate signaling pathways regulating human pancreas differentiation and morphogenesis, we developed a high-content, image-based screen and quantitative multivariate analysis pipelines robust to heterogeneity to extract single-cell and organoid features using pancreatic progenitor organoids. Here, we identified 54 compounds affecting cell identity and/or morphological landscape. Focusing on one family of compounds, we found that glycogen synthase kinase 3α/β (GSK3A/B) inhibition via wingless/int-1 (WNT) signaling has a reversible effect on cell identity, repressing pancreatic progenitor markers and inducing a poised state in progenitors transitioning to acinar cells. We show that additional fibroblast growth factor (FGF) repression enables further differentiation of acinar cells, recapitulating pancreatic acinar morphogenesis and function. The ability to produce acinar cells is valuable for future studies on pancreatic exocrine function and cancer initiation in humans, as acinar cells are thought to be an important cell of origin for pancreatic adenocarcinoma.
@article{Keshara9127,
author={Rashmiparvathi Keshara, Karolina Kuodyte, Antje Janosch, Cordula Andree, Marc Bickle, Martin Stöter, Rico Barsacchi, Yung Hae Kim, Anne Grapin-Botton},
title={High-content screening of organoids reveals the mechanisms of human pancreas acinar specification.},
journal ={Cell stem cell},
volume={33},
issue ={2},
pages={325--339},
year=2026
}

Jaakko I Lehtimäki#, Jingtao Lilue, Margarida R Cruz, Mario Del Rosario, Elisa Nerli, Ricardo Henriques, Caren Norden#
Spatiotemporal coordination of Slit-Robo repulsion and neurturin-Gfrα attraction guides multipolar migration during retinal lamination.
Cell Rep, 45(2) Art. No. 116948 (2026)
Open Access PubMed Source   

Multipolar migration is a conserved neuronal migration mode in the developing brain, enabling emerging neurons to navigate in crowded environments and reach precise laminar positions. Yet, how these cells interpret external cues to guide their migration is not fully understood. We investigate this question using retinal horizontal cells as a model. Combining transcriptomics, targeted CRISPR screening, and live imaging, we reveal the spatiotemporal guidance system underlying horizontal cell lamination: repulsive Slit1b/2-Robo2 signaling in the amacrine cell layer initiates apical horizontal cell migration, while attractive neurturin-Gfrα1/2 signaling from photoreceptors fine-tunes final positioning beneath the photoreceptor layer. Disruption of these pathways causes basal retention of horizontal cells, highlighting the importance of spatially coordinated signaling for proper lamination and functional retinal circuitry. Our results uncover how positional signals and tissue architecture cooperate to achieve neuronal migration precision, a principle likely relevant across the developing central nervous system.
@article{Lehtimäki9141,
author={Jaakko I Lehtimäki, Jingtao Lilue, Margarida R Cruz, Mario Del Rosario, Elisa Nerli, Ricardo Henriques, Caren Norden},
title={Spatiotemporal coordination of Slit-Robo repulsion and neurturin-Gfrα attraction guides multipolar migration during retinal lamination.},
journal ={Cell reports},
volume={45},
issue ={2},
pages={null--null},
year=2026
}

Jinjin Zhang, Xiuping Zhang, Ningyawen Liu, Jiang Hu, Michael Hiller, Virag Sharma, Fengming Han, He Dai, Xiaolong Tu, David N Cooper, Dong-Dong Wu, Lin Zeng
A POMT2 missense substitution contributes to hypoxia adaptation in hibernating mammals.
Mol Biol Evol, 43(2) Art. No. msag001 (2026)
Open Access PubMed Source   

Hibernation is an adaptive survival strategy used by animals to cope with extreme environmental conditions. Although this physiological process involves complex metabolic changes, its underlying biological mechanisms remain largely unknown. Through comparative genomic analysis of six hibernating species across five orders, we identified an ancient amino acid substitution in POMT2 (R708Q), exhibiting signals of both convergent and positive selection in hibernating mammals. Phylogenetic analysis using HeIST indicated hemiplasy as a possible explanation, though given mammalian divergence times and the broader evidence for convergence, this is best considered an alternative rather than the primary interpretation. Functional studies using transgenic mice demonstrated the contribution of this mutation to hypoxia adaptation. Notably, despite the absence of this mutation in Rodentia hibernators, we included Graphiurus kelleni as a positive control in physiological studies of transgenic mice carrying POMT2 (R708Q), given its remarkable hypoxia adaptation during hibernation. Our findings not only provide novel insights into the genetic basis of hypoxic adaptation in hibernating mammals but also suggest incomplete lineage sorting (hemiplasy) as a plausible evolutionary mechanism for this important adaptive trait.
@article{Zhang9125,
author={Jinjin Zhang, Xiuping Zhang, Ningyawen Liu, Jiang Hu, Michael Hiller, Virag Sharma, Fengming Han, He Dai, Xiaolong Tu, David N Cooper, Dong-Dong Wu, Lin Zeng},
title={A POMT2 missense substitution contributes to hypoxia adaptation in hibernating mammals.},
journal ={Molecular biology and evolution},
volume={43},
issue ={2},
pages={null--null},
year=2026
}

Hannes Ausserwöger, Rob Scrutton, Charlotte M Fischer, Tomas Sneideris, Daoyuan Qian, Ella de Csilléry, Ieva Baronaite, Kathrin Saar, Alan Z Białek, Marc Oeller, Georg Krainer, Titus Franzmann, Sina Wittmann, Juan M Iglesias-Artola, Gaetano Invernizzi, Anthony Hyman, Simon Alberti, Nikolai Lorenzen, Tuomas P J Knowles
Biomolecular condensates sustain pH gradients at equilibrium through charge neutralization.
Nat Chem, 18(2) 246-257 (2026)
Open Access PubMed Source   

Electrochemical gradients are essential to the functioning of cells and form across membranes using active transporters. Here we show in contrast that condensed biomolecular systems-often termed condensates-sustain pH gradients without any external energy input. By studying individual condensates on the micrometre scale using a microdroplet platform, we reveal dense-phase pH shifts towards conditions of minimal electrostatic repulsion. We demonstrate that protein condensates can drive substantial alkaline and acidic gradients, which are compositionally tunable and can extend to complex architectures sustaining multiple unique pH conditions simultaneously. Through in silico characterization of human proteomic condensate networks, we further highlight potential wide-ranging electrochemical properties emerging from condensation in nature, while correlating intracellular condensate pH gradients with complex biomolecular composition. Together, the emergent nature of condensation shapes distinct pH microenvironments, thereby creating a regulatory mechanism to modulate biochemical activity in living and artificial systems.
@article{Ausserwöger9136,
author={Hannes Ausserwöger, Rob Scrutton, Charlotte M Fischer, Tomas Sneideris, Daoyuan Qian, Ella de Csilléry, Ieva Baronaite, Kathrin Saar, Alan Z Białek, Marc Oeller, Georg Krainer, Titus Franzmann, Sina Wittmann, Juan M Iglesias-Artola, Gaetano Invernizzi, Anthony Hyman, Simon Alberti, Nikolai Lorenzen, Tuomas P J Knowles},
title={Biomolecular condensates sustain pH gradients at equilibrium through charge neutralization.},
journal ={Nature chemistry},
volume={18},
issue ={2},
pages={246--257},
year=2026
}

Alison Kickuth, Urša Uršič, Michael F Staddon, Jan Brugués
A mechanical ratchet drives unilateral cytokinesis.
Nature, 650(8102) 759-767 (2026)
Open Access PubMed Source   

The canonical mechanism that drives cell division comprises the formation and constriction of a contractile actin ring1-3. However, this mechanism is not compatible with the early development of many vertebrates4-9. Yolk-anchored embryos typically cannot form a complete ring during early cleavage divisions, but it remains unclear how a partial circular arc with loose ends can divide the cell. Here, by combining laser ablation of the cytokinetic band with rheological measurements in vivo, we show that stiffening of the bulk cytoplasm, mediated by the interphase microtubule network, stabilizes the contractile band by anchoring it along its length during growth. Conversely, as the cell cycle progresses, the cytoplasm fluidizes, diminishing band-cytoplasmic anchoring and facilitating band ingression. This dynamic interplay between stability and growth versus instability and ingression repeats for several cell cycles until division is complete, resulting in a mechanical ratchet that drives cell division. Our study underscores the role of temporal control over cytoplasmic rheology as a key feature that drives unilateral cytokinesis in the absence of a closed actin ring.
@article{Kickuth9124,
author={Alison Kickuth, Urša Uršič, Michael F Staddon, Jan Brugués},
title={A mechanical ratchet drives unilateral cytokinesis.},
journal ={Nature},
volume={650},
issue ={8102},
pages={759--767},
year=2026
}

Lei Yuan*, Sagarika Dawka*, Yohan Kim*, Anke Liebert*, Fabian Rost, Robert Arnes-Benito, Franziska Baenke, Christina Götz, David Long Hin Tsang, Andrea Schuhmann, Anna Shevchenko, Roberta Rezende de Castro, Seunghee Kim, Aleksandra Sljukic, Anna Dowbaj, Andrej Shevchenko, Daniel Seehofer, Dongho Choi, Georg Damm, Daniel E Stange, Meritxell Huch
Human assembloids recapitulate periportal liver tissue in vitro.
Nature, 650(8101) 438-449 (2026)
Open Access PubMed Source   

The development of complex multicellular human in vitro systems holds great promise for modelling disease and advancing drug discovery and tissue engineering1. In the liver, despite the identification of key signalling pathways involved in hepatic regeneration2,3, in vitro expansion of human hepatocytes directly from fresh patient tissue has not yet been achieved, limiting the possibility of modelling liver composite structures in vitro. Here we first developed human hepatocyte organoids (h-HepOrgs) from 28 different patients. Patient-derived hepatocyte organoids sustained long-term expansion of hepatocytes in vitro and maintained patient-specific gene expression and bile canaliculus features and function of the in vivo tissue. After transplantation, expanded h-HepOrgs rescued the phenotype of a mouse model of liver disease. By combining h-HepOrgs with portal mesenchyme and our previously published cholangiocyte organoids4-6, we generated patient-specific periportal liver assembloids that retain the histological arrangement, gene expression and cell interactions of periportal liver tissue, with cholangiocytes and mesenchyme embedded in the hepatocyte parenchyma. We leveraged this platform to model aspects of biliary fibrosis. Our human periportal liver assembloid system represents a novel in vitro platform to investigate human liver pathophysiology, accelerate drug development, enable early diagnosis and advance personalized medicine.
@article{Yuan9100,
author={Lei Yuan, Sagarika Dawka, Yohan Kim, Anke Liebert, Fabian Rost, Robert Arnes-Benito, Franziska Baenke, Christina Götz, David Long Hin Tsang, Andrea Schuhmann, Anna Shevchenko, Roberta Rezende de Castro, Seunghee Kim, Aleksandra Sljukic, Anna Dowbaj, Andrej Shevchenko, Daniel Seehofer, Dongho Choi, Georg Damm, Daniel E Stange, Meritxell Huch},
title={Human assembloids recapitulate periportal liver tissue in vitro.},
journal ={Nature},
volume={650},
issue ={8101},
pages={438--449},
year=2026
}
* joint first authors, # joint corresponding authors