@phdthesis{20964, author = {Vladimirtsev, Dmitrii}, issn = {2791-4585}, pages = {22}, publisher = {Institute of Science and Technology Austria}, title = {{Armadillo repeat only proteins are master regulators of plant cyclic-nucleotide gated channels}}, doi = {10.15479/AT-ISTA-20964}, 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}, } @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= {{Data associated with Keratins coordinate tissue spreading }}, doi = {10.15479/AT-ISTA-21137}, year = {2026}, } @unpublished{21291, abstract = {The complexity and specificity of movement in vertebrates is driven by a rich diversity of spinal motor and interneuron cell types. During development, eleven spinal cord progenitor domains generate an equivalent number of cardinal neuron types. How progenitor domains, individual progenitors, and post-mitotic diversity relate is still unknown. We performed high-resolution, single-progenitor cell lineage tracing in the embryonic mouse spinal cord using mosaic analysis with double markers (MADM). Our quantitative study of lineage progression revealed that spinal cord progenitors undergo highly variable numbers of proliferative, neurogenic, and gliogenic cell divisions. The nascent clonally-related neurons migrate radially over large distances, span the dorsoventral axis, and even cross the midline, demonstrating striking bilaterality. Molecular and morphometric analysis indicate high levels of progenitor multipotency, with an individual progenitor capable of producing several molecularly and morphologically distinct neuron types, as well as astrocytes. These findings redefine spinal cord development as a process in which lineage variability — rather than rigid progenitor identity — drives the generation of cellular diversity.}, author = {Gobeil, Sophie A and Da Silveira Neto, Francisco and Silvestrelli, Giulia and Smits, Matthijs Geert and Streicher, Carmen and Cheung, Giselle T and Hippenmeyer, Simon and Sweeney, Lora Beatrice Jaeger}, booktitle = {bioRxiv}, title = {{Lineage origin of spinal cord cell type diversity}}, doi = {10.64898/2026.02.12.705305}, year = {2026}, } @article{21382, abstract = {The exceptional energy-harvesting efficiency of lead-halide perovskites arises from unusually long photocarrier diffusion lengths and recombination lifetimes that persist even in defect-rich, solution-grown samples. Paradoxically, perovskites are also known for having very short exciton decay times. Here, we resolve this apparent contradiction by showing that key optoelectronic properties of perovskites can be explained by localized flexoelectric polarization confined to interfaces between domains of spontaneous strain. Using birefringence imaging, electrochemical staining, and zero-bias photocurrent measurements, we visualize the domain structure and directly probe the associated internal fields in nominally cubic single crystals of methylammonium lead bromide. We demonstrate that localized flexoelectric fields spatially separate electrons and holes to opposite sides of domain walls, exponentially suppressing recombination. Domain walls thus act as efficient mesoscopic transport channels for long-lived photocarriers, microscopically linking structural heterogeneity to charge transport and offering mechanistically informed design principles for perovskite solar-energy technologies.}, author = {Rak, Dmytro and Lorenc, Dusan and Balazs, Daniel and Zhumekenov, Ayan A. and Bakr, Osman M. and Alpichshev, Zhanybek}, issn = {2041-1723}, journal = {Nature Communications}, publisher = {Springer Nature}, title = {{Flexoelectric domain walls enable charge separation and transport in cubic perovskites}}, doi = {10.1038/s41467-026-68660-5}, volume = {17}, year = {2026}, } @article{21490, abstract = {Auxin canalization is a self-organizing process that governs the flexible formation of vasculature by reinforcing the formation of auxin transport channels. A key prerequisite is the feedback between auxin signaling and directional auxin transport, mediated by PIN transporters. Despite the developmental importance of canalization, the molecular components linking auxin perception to the regulation of PIN auxin transporters remain poorly understood. Here, we identify TOW, a novel and essential component of auxin canalization that links intracellular auxin signaling with cell surface auxin perception. TOW is regulated downstream of TIR1/AFB-Aux/IAA-WRKY23 transcriptional auxin signaling. tow mutants exhibit defects in regeneration and de novo vasculature formation, along with impaired formation of polarized, PIN-expressing auxin channels. At the subcellular level, these mutants display disrupted auxin-induced PIN polarization and altered PIN endocytic trafficking dynamics. TOW localizes predominantly to the plasma membrane, where it interacts with receptor-like kinases involved in auxin canalization, including the TMK1 auxin co-receptor and the CAMEL-CANAR complex. TOW promotes PIN interaction with these kinases and stabilizes PINs at the cell surface. Together, our findings identify TOW as a molecular link between intracellular and cell surface auxin signaling mechanisms that converge on PIN trafficking and polarity, providing new insights into how auxin signaling regulates directional auxin transport for the self-organizing formation of vasculature during flexible plant development.}, author = {Li, Mingyue and Rydza, Nikola and Mazur, Ewa and Molnar, Gergely and Nodzyński, Tomasz and Friml, Jiří}, issn = {0960-9822}, journal = {Current Biology}, number = {6}, pages = {1468--1480.e6}, publisher = {Elsevier}, title = {{Receptor-like-kinase-interacting protein TOW stabilizes PIN transporters for auxin canalization}}, doi = {10.1016/j.cub.2026.02.023}, volume = {36}, year = {2026}, } @article{21746, abstract = {As vertebrates transitioned from water to land, locomotion shifted from undulatory swimming to limb-based movement. How spinal circuits and their cell types evolved to support this transition remains unclear. We leverage frog metamorphosis, which recapitulates this transition within a single organism, to define how spinal circuits generate aquatic versus terrestrial motor patterns. At swim stages, spinal architecture is uniform, with a transcriptionally and anatomically homogeneous motor and interneurons. As limbs develop and their movement complexifies, spinal circuits expand in neuron number and subtype diversity. This expansion is most pronounced for V1 inhibitory neurons, which increase ∼70-fold and diversify into transcriptionally distinct subtypes. Disrupting transcription factors defining emerging motor and V1 populations reveals molecular segregation between swim and limb circuits, highlighting the role of subtype diversity in motor coordination. A multifold increase in inhibitory neuron diversity thus underlies the tail-to-limb locomotor transition, providing a framework for spinal circuit adaptation during vertebrate evolution.}, author = {Vijatovic, David and Toma, Florina Alexandra and Ignatyev, Y and Harrington, Zoe P and Sommer, Christoph M and Hauschild, Robert and Smits, Matthijs Geert and Dalla Vecchia, Marco and Trevisan, Alexandra J. and Chapman, Phillip and Julseth, Mara and Brenner-Morton, Susan and Gabitto, Mariano I. and Dasen, Jeremy S. and Bikoff, Jay B. and Sweeney, Lora Beatrice Jaeger}, issn = {2211-1247}, journal = {Cell Reports}, number = {4}, publisher = {Elsevier}, title = {{Multifold increase in spinal inhibitory cell types with emergence of limb movement}}, doi = {10.1016/j.celrep.2026.117227}, volume = {45}, year = {2026}, } @article{21762, abstract = {Bacteria, like eukaryotes, use conserved cytoskeletal systems for intracellular organization. The plasmid-encoded ParMRC system forms actin-like filaments that segregate low–copy number plasmids. In multicellular cyanobacteria such as Anabaena sp., we found that a chromosomally encoded ParMR system has evolved into a cytoskeletal system named CorMR with a function in cell shape control rather than DNA segregation. Live-cell imaging, in vitro reconstitution, and cryo–electron microscopy revealed that CorM formed dynamically unstable, antiparallel double-stranded filaments that were recruited to the membrane by CorR through an amphipathic helix conserved in multicellular cyanobacteria. CorMR filaments were regulated by MinC, which excluded them from the poles and division plane. Comparative genomics indicated that the repurposing of ParMR and Min systems coevolved with cyanobacterial multicellularity, highlighting the evolutionary plasticity of cytoskeletal systems in bacteria.}, author = {Springstein, Benjamin L and Javoor, Manjunath and Megrian, Daniela and Hajdu, Roman and Hanke, Dustin M. and Zens, Bettina and Weiss, Gregor L. and Schur, Florian Km and Loose, Martin}, issn = {1095-9203}, journal = {Science}, number = {6795}, publisher = {AAAS}, title = {{Repurposing of a DNA segregation machinery into a cytoskeletal system controlling cell shape}}, doi = {10.1126/science.aea6343}, volume = {392}, year = {2026}, } @article{21763, abstract = {Reactive oxygen species (ROS) have been implicated in multiple signaling processes in plants, but the underlying mechanisms and roles remain enigmatic. In this study, we developed a method of live imaging of apoplastic ROS at the root surface. Distinct signals, including auxin, extracellular adenosine triphosphate, and rapid alkalinization factor 1 peptide, induce cytosolic calcium transients and apoplastic ROS bursts. Genetic and optogenetic manipulations of Arabidopsis identified calcium transients as necessary and sufficient for ROS bursts through activation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidases RBOHC and RBOHF. Apoplastic ROS bursts are not required, but they do limit gravity-induced root bending. Root bending is sensed by the stretch-activated calcium channel MCA1, leading to NADPH oxidase activation. The resulting ROS production stiffens cell walls to facilitate soil penetration. Apoplastic ROS thus provides a means to balance tissue flexibility and stiffness to navigate soil.}, author = {Kulich, Ivan and Vladimirtsev, Dmitrii and Randuch, Marek and Gao, Shiqiang and Citterico, Matteo and Konrad, Kai R. and Nagel, Georg and Wrzaczek, Michael and Cascaro, Léa and Vinet, Pauline and Durand, Pauline and Asnacios, Atef and Verma, Lokesh and Bennett, Malcolm J. and Pandey, Bipin K. and Friml, Jiří}, issn = {1095-9203}, journal = {Science}, number = {6795}, pages = {296--300}, publisher = {AAAS}, title = {{Calcium-triggered apoplastic ROS bursts balance gravity and mechanical signals for soil navigation}}, doi = {10.1126/science.adu8197}, volume = {392}, year = {2026}, } @unpublished{21962, abstract = {The generation of faithful cell-type diversity and correct projection neuron numbers is essential for cerebral cortex development. Corticogenesis is however susceptible to genetic interference of critical signaling pathways, including mutations in Mtor/Rptor that lead to microcephaly. How the loss of Rptor/mTORC1 function affects cortical developmental programs, at single cell level, is still unknown. Here, we utilized Mosaic Analysis with Double Markers (MADM) technology to probe Rptor gene function upon sparse single cell- or global tissue-wide ablation. We found that tissue-wide effects drive the etiology of cortical microcephaly upon loss of Rptor, rather than deficits in projection neuron genesis. Conversely, Rptor function is cell-autonomously required for postnatal projection neuron survival in a highly cell-type-specific manner. Collectively, our results suggest that the fine balance of precise cell-type-specific cell-autonomous Rptor/mTORC1 function in concert with non-cell-autonomous tissue-wide effects is essential for the development of a properly-sized cerebral cortex with accurate projection neuron diversity.}, author = {Villalba Requena, Ana and Beattie, Robert J and Pauler, Florian and Streicher, Carmen and Miranda, Osvaldo and Krausgruber, Thomas and Senekowitsch, Martin and Farlik, Matthias and Bock, Christoph and Rülicke, Thomas and Hippenmeyer, Simon}, booktitle = {bioRxiv}, title = {{Mtor/Rptor function globally prevents cortical microcephaly and cell-autonomously promotes postnatal neuron survival in cell type specific manner}}, doi = {10.64898/2026.05.01.722172}, year = {2026}, } @unpublished{21963, abstract = {The cerebral cortex consists of immense numbers of neuronal and glial cell-types derived from radial glial progenitor (RGP) cells. How RGPs generate appropriate quantities of distinct cortical cell-types to safeguard a brain of correct size, is not well understood. However, genetic aberration in human, including mutations in PTEN, lead to cortical malformation such as macrocephaly, albeit with unknown etiology. Here we utilized Mosaic Analysis with Double Markers (MADM)-based clonal analysis and single cell phenotyping to decipher the role of Pten in neurogenic and gliogenic RGP lineage progression during cortical ontogeny. While neurogenic RGP lineage progression and projection neuron production was moderately altered in the absence of Pten, cortical astrocyte production was drastically increased. Through genetic epistasis experiments we show that the loss of Pten uncouples astrocyte generation from essential growth factor signaling hubs, funneling into MAPK. Collectively, our results suggest that Pten regulates RGP lineage progression with distinct sequential functions in cortical projection neurogenesis and astrocyte production to ensure the emergence of a correctly-sized cerebral cortex.}, author = {Miranda, Osvaldo and Contreras, Ximena and Pauler, Florian and Davaatseren, Amarbayasgalan and Amberg, Nicole and Streicher, Carmen and Villalba Requena, Ana and Heger, Anna-Magdalena and Marie, Corentine and Hassan, Bassem A. and Rülicke, Thomas and Hippenmeyer, Simon}, booktitle = {bioRxiv}, title = {{Pten orchestrates neurogenic radial glia lineage progression and tunes neocortical astrocyte production}}, doi = {10.64898/2026.05.01.722191}, year = {2026}, } @article{22229, abstract = {Hippocampal CA3 pyramidal neurons (PNs) form the largest autoassociative network in the mammalian brain. Whether CA3–CA3 recurrent connectivity is genetically preconfigured or environmentally shaped during ongoing memory storage is currently unknown. To address this question, we performed multicellular patch-clamp-based circuit mapping of up to eight CA3 PNs in the mouse hippocampus at multiple postnatal time points (P7–8, P18–25, and P45–50). Here, we show that the hippocampal CA3 network undergoes a developmental transformation from local, dense, and random connectivity to a distributed, sparse, and structured configuration. Thus, sparse and structured connectivity may emerge via experience-dependent mechanisms. In parallel, the strength of single synapses is downregulated; single synaptic events are sufficient to trigger postsynaptic spiking early in development, whereas spatial summation of several inputs is required at later time points. Biologically inspired models of memory storage by Hebbian synaptic plasticity and retrieval via pattern completion suggest that developmental changes improve specific aspects of memory storage and retrieval. Our results imply a developmental transformation of the neuronal code and the memory functions in the hippocampal CA3 network.}, author = {Vargas Barroso, Victor M and Watson, Jake and Navas Olivé, Andrea C and Schlögl, Alois and Jonas, Peter M}, issn = {2041-1723}, journal = {Nature Communications}, publisher = {Springer Nature}, title = {{Developmental emergence of sparse and structured synaptic connectivity in the hippocampal CA3 memory circuit}}, doi = {10.1038/s41467-026-71914-x}, volume = {17}, year = {2026}, } @misc{21439, abstract = {These files contain supplementary movies accompanying the PhD thesis “Geometry-driven self-organization of migrating cells and chiral filaments” by Zuzana Dunajova (2026). The videos provide additional visual material supporting the experiments and results described in the thesis.}, author = {Dunajova, Zuzana}, publisher = {Institute of Science and Technology Austria}, title = {{Supplementary movies to PhD thesis “Geometry-driven self-organization of migrating cells and chiral filaments”}}, doi = {10.15479/AT-ISTA-21439}, year = {2026}, } @article{21161, abstract = {In many species, sex-biased expression is widespread and thought to contribute to sexual dimorphism. While bulk RNA-sequencing has been instrumental in identifying strongly sex-biased genes, it lacks resolution to assess variation across cell-types and tissue compartments. Using single-nucleus expression data from the Fly Cell Atlas, we investigate sex differences in adult Drosophila melanogaster. We find that differences in cell-type composition between the sexes are not a major source of sex-bias, as for the vast majority of genes, the degree of sex-bias is similar regardless of whether sex differences in cell-type composition are controlled for or not. Our analysis confirms a deficit of X-linked male-biased genes in the body’s somatic tissues that is widespread across cell-types. We also find the excess of X-linked female-biased genes to be associated with nervous system cells in the head but with epithelial cells in the body’s somatic tissues, showing that single-nucleus data crucially resolves sex-bias at the cell-type level. We investigate dosage compensation (DC) across 15 tissues and 17 cell-types. We observe that it varies throughout the body. Surprisingly, we observe a lack of DC in a cluster of main cells within the male accessory glands. This result highlights the importance of understanding context-dependent DC.}, author = {De Castro Barbosa Rodrigues Barata, Carolina and Vicoso, Beatriz}, issn = {1471-2954}, journal = {Proceedings of the Royal Society B Biological Sciences}, number = {2063}, publisher = {Royal Society of London}, title = {{Single-nucleus resolution of sex-biased expression and dosage compensation in Drosophila melanogaster}}, doi = {10.1098/rspb.2025.2471}, volume = {293}, year = {2026}, } @article{22295, abstract = {Despite the functional diversity of over 100 causal genes1,2,3, phenotypic convergence across models may reveal common neurobiological processes in autism spectrum disorder (ASD). Here we profiled 251 samples from 11 monogenic mouse models of ASD using single-nucleus multi-omic sequencing across three developmental stages, both sexes and two brain regions. Despite genetic heterogeneity, ASD-linked mutations converged on perturbations of the radial glial cell lineage. These alterations reflect a transient developmental delay rather than lasting lineage misspecification and resolve by postnatal stages. Molecularly, the largest transcriptional differences emerged in neurons at early postnatal stages. These changes included downregulation of synaptic and ion channel-related genes, consistent with homeostatic adaptation or delayed maturation. Network analysis showed molecular convergence across models within each developmental stage, suggesting that diverse mutations linked to ASD impinge on common, stage-specific processes. Convergence becomes less pronounced by postnatal day 14, highlighting the dynamic nature of ASD-associated changes. Cross-genotype heterogeneity is superimposed on stage-specific effects. Electrophysiology corroborated this pattern: mutants generally showed altered neuronal excitability and synaptic properties with model-specific nuances. Our study also highlighted sex-specific gene expression alterations, with female mice often displaying larger effect sizes than male mice. Together, our findings provide a comprehensive view of developmental cellular and molecular dynamics across models of ASD.}, author = {Schwarz, Lena A and Dotter, Christoph and Isaev, Sergey and Lisi, Michela and Malzl, Daniel and Büschl, Christoph and Ladstätter, Sabrina and Oliveira, Bárbara and Barel, Matteo and Basilico, Bernadette and Chintaluri, Chaitanya and Gorkiewicz, Sarah and Goudarzi, Mohammad and Belinova, Tereza and Reichl, Stephan and Sendžikaitė, Gintarė and Arcot Jayaram, Satish and Koppensteiner, Peter and Sommer, Christoph M and Vogels, Tim P and Menche, Jörg and Adameyko, Igor and Kharchenko, Peter Vasili and Bock, Christoph and Novarino, Gaia}, issn = {1476-4687}, journal = {Nature}, publisher = {Springer Nature}, title = {{Cortical development dynamics across autism spectrum disorder mouse models}}, doi = {10.1038/s41586-026-10679-1}, year = {2026}, } @article{22301, abstract = {Auxin, primarily indole-3-acetic acid (IAA), is a central regulator of growth and development in land plants, but its physiological role in chlorophyte algae remains unclear. Here, we show that exogenous IAA modulates growth in Chlorella sorokiniana, Chlorella variabilis, and Chlamydomonas reinhardtii in a concentration-dependent manner. Low IAA concentrations promoted growth by accelerating the onset of cell division without affecting cell size, whereas higher concentrations inhibited proliferation. Radiotracer assays showed that all three species take up and release IAA across the plasma membrane through a combination of passive diffusion and energy-dependent, saturable processes. Competition by excess unlabeled natural and synthetic auxins further supported the presence of carrier-mediated transport with broad substrate recognition. Phylogenetic analyses identified potential PIN-like auxin exporters in chlorophytes and other non-plant eukaryotes, and structural modeling supported conservation of the overall PIN fold and predicted auxin-binding residues. However, functional assays in Xenopus laevis oocytes, tobacco BY-2 cultured cells, and Arabidopsis thaliana did not support a role for these proteins in directional auxin export. Instead, non-plant PIN homologs localized predominantly to the endoplasmic reticulum and showed limited or no transport activity in heterologous systems. Together, these findings indicate that auxin responsiveness and basic cellular auxin transport predate canonical PIN-mediated directional auxin export, which appears to be a later innovation of the streptophyte lineage.}, author = {Smoljan, Adrijana and Koutnik‐Abele, Sarah and Vladimirtsev, Dmitrii and Klíma, Petr and Bírošíková, Anita and Zhang, Yuzhou and Merrin, Jack and Schuster, Maximilian and Kurtović, Katarina and Hammes, Ulrich Z. and Petrášek, Jan and Friml, Jiří}, issn = {1744-7909}, journal = {Journal of Integrative Plant Biology}, publisher = {Wiley}, title = {{Auxin response and PIN‐mediated transport in chlorophyte algae}}, doi = {10.1111/jipb.70309}, year = {2026}, } @unpublished{22276, abstract = {Tissue tension is a key determinant of tissue shape, and its regulation is essential for both morphogenesis and the maintenance of tissue integrity. During zebrafish embryogenesis, the enveloping layer (EVL) – an epithelial monolayer covering the blastoderm – undergoes extensive spreading that is driven by pulling forces exerted at its margin and more than doubles its surface area. Yet whether and how the EVL actively regulates its tissue tension during this process remains unclear. Here, we show that the EVL maintains constant tissue tension while spreading, and that it achieves this by reducing apical cell contractility in response to the same pulling forces that drive its spreading. We identify a mechanosensitive pathway underlying this response, mediated by the scaffold/adaptor protein Kibra regulating the activity of atypical protein kinase C (aPKC) at the apical domain of EVL cells. Under low mechanical stretch, Kibra forms condensates at the base of actin-based apical projections, where it activates Myosin II to increase apical contractility through aPKC downregulation. As mechanical stretch increases, apical projections disassemble, Kibra condensates dissolve, and aPKC activity rises. Elevated aPKC activity in turn reduces apical contractility by reducing Myosin II activity, thereby maintaining constant tissue tension despite increased mechanical stretch. Together, these findings reveal a mechanosensitive mechanism that enables robust adaptation of tissue tension to changing mechanical stretch, ensuring efficient tissue spreading and morphogenesis.}, author = {Hino, Naoya and Kapoor, Tushna and Gubbala, Uday R and Hannezo, Edouard B and Heisenberg, Carl-Philipp J}, keywords = {Epithelial spreading, tissue tension, mechanosensation, aPKC, Kibra, zebrafish}, publisher = {Institute of Science and Technology Austria}, title = {{Apical domain mechanosensation regulates tissue tension homeostasis}}, year = {2026}, } @article{22371, abstract = {Amoeboid cell migration is key to efficient T cell immunity. Spatial polarization of organelles within cells, including endo-lysosomes, is a prerequisite of migration. However, how ultrastructural polarization is linked to the signaling requirements governing T cell migration remains unknown. Here we show that signaling molecules generated by endo-lysosome-localized kinases regulate velocity of amoeboid migration. Specifically, imaging of T cells identifies accumulation of endo-lysosomes decorated with the lipid kinases VPS34–PIKfyve at the uropod of polarized cells. Activity of VPS34 and PIKfyve regulates speed, but not directedness, of migrating T cells. Mechanistically, PI(3,5)P2 generated by the sequential action of VPS34 and PIKfyve, mediates Ca2+ efflux from lysosomes via the mucolipin TRP cation channel 1 (TRPML1), thus controlling activity of myosin IIA and hence the generation of propulsive force through retrograde actin flow. The VPS34–PIKfyve kinases also regulate velocity of myeloid cells, as well as of the amoeba Dictyostelium discoideum – establishing the axis as an evolutionarily conserved speed control system of amoeboid cell migration.}, author = {Dehio, Philippe G and Michard, Céline and Yam-Puc, Juan Carlos and Martí I Líndez, Adrià Arnau and Jandke, Anett and Unterstab, Gunhild and Fabre, Lucien and Sauteur, Loïc and Artinger, Marc and Legler, Daniel F. and Sixt, Michael K and Schaefer, Thorsten and Wymann, Matthias P. and Okkenhaug, Klaus and Soldati, Thierry and Mehling, Matthias and Hess, Christoph}, issn = {1469-3178}, journal = {EMBO Reports}, publisher = {Springer Nature}, title = {{A conserved VPS34-PIKfyve-TRPML1-myosin II axis regulates the speed of amoeboid cell migration}}, doi = {10.1038/s44319-026-00861-x}, year = {2026}, } @article{21883, abstract = {Three-dimensional (3D) printing has rapidly developed from a niche hobbyist activity into a widely accessible and indispensable technology across multiple scientific disciplines. Within microscopy, optical engineering laboratories and imaging core facilities, 3D printing enables creating customised solutions for sample holders, optical components and everyday laboratory tools that traditionally required specialised machining. By providing rapid prototyping, low-cost production and reproducibility, 3D printing facilitates innovation and efficiency in facility operations. This article provides a perspective on the possibilities, challenges, and practical aspects of implementing 3D printing within microscopy core facilities. Instead of providing technical review about 3D printing, we focus on service organisation, user engagement, resource management and community-driven repositories for design dissemination. Our aim is to share insights with those considering the implementation of 3D printing as a service for developing add-on components to ease the operation of different aspects of the machine-park driven services and those who are managing advanced instrumentation within research groups.}, author = {Goudarzi, Mohammad and Schuster, Maximilian and Milberger, Arthur and Gunkel, Manuel and Terjung, Stefan and Krens, Gabriel}, issn = {1365-2818}, journal = {Journal of Microscopy}, number = {3}, pages = {382--395}, publisher = {Wiley}, title = {{3D printing in core facilities – Low pain, high gain}}, doi = {10.1111/jmi.70106}, volume = {302}, year = {2026}, } @phdthesis{21360, author = {Riegler, Stefan}, issn = {2663-337X}, pages = {185}, publisher = {Institute of Science and Technology Austria}, title = {{Root system plasticity under nutrient limitation: Investigating hormonal and molecular drivers in Arabidopsis thaliana and Coffea species}}, doi = {10.15479/AT-ISTA-21360}, year = {2026}, }