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Giovanni Volpe, Carolina Wählby, Lei Tian, Michael Hecht, Artur Yakimovich, Kristina Monakhova, Laura Waller, Ivo F. Sbalzarini, Christopher A Metzler, Mingyang Xie, Kevin Zhang, Isaac C D Lenton, Halina Rubinsztein-Dunlop, Daniel Brunner, Bijie Bai, Aydogan Ozcan, Daniel Midtvedt, Hao Wang, Nataša Sladoje, Joakim Lindblad, Jason T Smith, Marien Ochoa, Margarida Barroso, Xavier Intes, Tong Qiu, Li-Yu Yu, Sixian You, Yongtao Liu, Maxim A Ziatdinov, Sergei V Kalinin, Arlo Sheridan, Uri Manor, Elias Nehme, Ofri Goldenberg, Yoav Shechtman, Henrik K Moberg, Christoph Langhammer, Barbora Špačková, Saga Helgadottir, Benjamin Midtvedt, Aykut Argun, Tobias Thalheim, Frank Cichos, Stefano Bo, Lars Hubatsch, Jesus Pineda, Carlo Manzo, Harshith Bachimanchi, Erik Selander, Antoni Homs-Corbera, Martin Fränzl, Kevin de Haan, Yair Rivenson, Zofia Korczak, Caroline Beck Adiels, Mite Mijalkov, Dániel Veréb, Yu-Wei Chang, Joana B Pereira, Damian Matuszewski, Gustaf Kylberg, Ida-Maria Sintorn, Juan C Caicedo, Beth A Cimini, Muyinatu A Lediju Bell, Bruno M Saraiva, Guillaume Jacquemet, Ricardo Henriques, Wei Ouyang, Trang Le, Estibaliz Gómez-de-Mariscal, Daniel Sage, Arrate Muñoz-Barrutia, Ebba Josefson Lindqvist, Johanna Bergman
Roadmap on Deep Learning for Microscopy.
J. Phys. Photonics, 8(1) Art. No. 012501 (2026)
Open Access   PubMed Source   

Through digital imaging, microscopy has evolved from primarily being a means for visual observation of life at the micro- and nano-scale, to a quantitative tool with ever-increasing resolution and throughput. Artificial intelligence, deep neural networks, and machine learning (ML) are all niche terms describing computational methods that have gained a pivotal role in microscopy-based research over the past decade. This Roadmap encompasses key aspects of how ML is applied to microscopy image data, with the aim of gaining scientific knowledge by improved image quality, automated detection, segmentation, classification and tracking of objects, and efficient merging of information from multiple imaging modalities. We aim to give the reader an overview of the key developments and an understanding of possibilities and limitations of ML for microscopy. It will be of interest to a wide cross-disciplinary audience in the physical sciences and life sciences.
@article{Volpe9134,
author={Giovanni Volpe, Carolina Wählby, Lei Tian, Michael Hecht, Artur Yakimovich, Kristina Monakhova, Laura Waller, Ivo F. Sbalzarini, Christopher A Metzler, Mingyang Xie, Kevin Zhang, Isaac C D Lenton, Halina Rubinsztein-Dunlop, Daniel Brunner, Bijie Bai, Aydogan Ozcan, Daniel Midtvedt, Hao Wang, Nataša Sladoje, Joakim Lindblad, Jason T Smith, Marien Ochoa, Margarida Barroso, Xavier Intes, Tong Qiu, Li-Yu Yu, Sixian You, Yongtao Liu, Maxim A Ziatdinov, Sergei V Kalinin, Arlo Sheridan, Uri Manor, Elias Nehme, Ofri Goldenberg, Yoav Shechtman, Henrik K Moberg, Christoph Langhammer, Barbora Špačková, Saga Helgadottir, Benjamin Midtvedt, Aykut Argun, Tobias Thalheim, Frank Cichos, Stefano Bo, Lars Hubatsch, Jesus Pineda, Carlo Manzo, Harshith Bachimanchi, Erik Selander, Antoni Homs-Corbera, Martin Fränzl, Kevin de Haan, Yair Rivenson, Zofia Korczak, Caroline Beck Adiels, Mite Mijalkov, Dániel Veréb, Yu-Wei Chang, Joana B Pereira, Damian Matuszewski, Gustaf Kylberg, Ida-Maria Sintorn, Juan C Caicedo, Beth A Cimini, Muyinatu A Lediju Bell, Bruno M Saraiva, Guillaume Jacquemet, Ricardo Henriques, Wei Ouyang, Trang Le, Estibaliz Gómez-de-Mariscal, Daniel Sage, Arrate Muñoz-Barrutia, Ebba Josefson Lindqvist, Johanna Bergman},
title={Roadmap on Deep Learning for Microscopy.},
journal ={Journal of Physics: Photonics},
volume={8},
issue ={1},
pages={null--null},
year=2026
}

Cordula Reuther*, Paula Santos-Otte*, Rahul Grover, Till Korten, Stefan Diez
Microtubule lattice defects facilitate spastin-mediated severing.
J Cell Sci, Art. No. doi: 10.1242/jcs.264497 (2026)
Open Access PubMed Source   

The length regulation of microtubules and their organization into complex arrays inside cells occurs through the activity of polymerases, depolymerases as well as severing enzymes such as spastin and katanin. The latter hexamerize on the microtubule lattice, pull out single tubulin dimers in an ATP-dependent manner and eventually generate internal breaks in the microtubule. While spastin was shown to be regulated by posttranslational tubulin modifications, the impact of microtubule lattice defects on the severing characteristics of spastin has not been explored. To answer this question, we prepared GMPCPP-stabilized microtubules with varying defect densities - introduced either through specific polymerization conditions or by end-to-end annealing - for subsequent in vitro severing assays. We found that (i) the presence of defects accelerated the onset of the severing process and (ii) severing was twice as frequent in microtubule segments with defect sites as compared to random lattice segments. However, there was no evidence of preferential binding of spastin to defect sites. We therefore propose a severing mechanism in which defects do not actively promote microtubule severing but rather passively contribute to microtubule lattice instability, facilitating the process as fewer tubulin subunits are required to be removed for microtubule severing.
@article{Reuther9150,
author={Cordula Reuther, Paula Santos-Otte, Rahul Grover, Till Korten, Stefan Diez},
title={Microtubule lattice defects facilitate spastin-mediated severing.},
journal ={Journal of cell science},
volume={},
pages={1--1},
year=2026
}

C Darrin Hulsey, Paolo Franchini, Paul Masonick, Andreas F Kautt, Gonzalo Machado-Schiaffino, Martin Pippel, Francisco J García-de León, Eugene W Myers, Axel Meyer
Divergence at the IRX gene cluster underlies extreme trophic polymorphism in a cichlid fish (Herichthys minckleyi).
Commun Biol, Art. No. doi: 10.1038/s42003-026-09689-6 (2026)
Open Access PubMed Source   

The origin of the extensive phenotypic divergence characterizing adaptive radiation could often be geographically localized and genetically simple. In a classic case of a trophically polymorphic cichlid fish (Herichthys minckleyi), we investigated alternative genomic processes that could have produced its extreme within-population variation in pharyngeal jaw tooth size. First, we generated a high-quality reference genome for its close relative (H. cyanoguttatus) to dissect the genetic architecture of this dental polymorphism. Then, using whole genome resequencing across the small Cuatro Ciénegas valley where H. minckleyi is endemic, we found substantial micro-geographic subdivision and effectively no genetic structure due to pharyngeal morphotype. We also employed quantitative trait loci mapping and genome wide association to pinpoint a single peak in an Iroquois-related (IRX) gene cluster associated with H. minckleyi's dental divergence. Interspecific introgression in this genomic region appears negligible, suggesting the genomic basis of the polymorphism likely arose within cichlids confined to Cuatro Ciénegas. Because H. minckleyi tooth size disparity is comparable to that found in all Central American cichlids, this offers a striking example of how genomic divergence at a single locus could produce a punctuated burst of eco-morphological divergence that generates phenotypic breadth comparable to a highly diverse cichlid adaptive radiation.
@article{Hulsey9151,
author={C Darrin Hulsey, Paolo Franchini, Paul Masonick, Andreas F Kautt, Gonzalo Machado-Schiaffino, Martin Pippel, Francisco J García-de León, Eugene W Myers, Axel Meyer},
title={Divergence at the IRX gene cluster underlies extreme trophic polymorphism in a cichlid fish (Herichthys minckleyi).},
journal ={Communications biology},
volume={},
pages={1--1},
year=2026
}

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
}

Gaelen Guzman, André Nadler, Frank Stein, Jeremy M Baskin, Carsten Schultz, Fikadu G Tafesse
The Lipid Interactome: an interactive and open access platform for exploring cellular lipid-protein interactions.
Bioinformatics, 42(2) Art. No. btaf651 (2026)
Open Access PubMed Source   

Lipid-protein interactions play essential roles in cellular signaling and membrane dynamics, yet their systematic characterization has long been hindered by the inherent biochemical properties of lipids. Recent advances in functionalized lipid probes-equipped with photoactivatable crosslinkers, affinity handles, and photocleavable protecting groups-have enabled proteomics-based identification of lipid interacting proteins with unprecedented specificity and resolution. Despite the growing number of published lipid interactomes, there remains no centralized effort to harmonize, compare, or integrate these datasets. The Lipid Interactome addresses this gap by providing a structured, interactive web portal that adheres to FAIR data principles-ensuring that lipid interactome studies are Findable, Accessible, Interoperable, and Reusable. Through standardized data formatting, interactive visualizations, and direct cross-study comparisons, this resource enables researchers to systematically explore the protein-binding partners of diverse bioactive lipids. By consolidating and curating lipid interactome proteomics data from multiple studies, the Lipid Interactome database serves as a critical tool for deciphering the biological functions of lipids in cellularsystems.
@article{Guzman9153,
author={Gaelen Guzman, André Nadler, Frank Stein, Jeremy M Baskin, Carsten Schultz, Fikadu G Tafesse},
title={The Lipid Interactome: an interactive and open access platform for exploring cellular lipid-protein interactions.},
journal ={Bioinformatics (Oxford, England)},
volume={42},
issue ={2},
pages={null--null},
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
}
* joint first authors, # joint corresponding authors