@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}, } @article{21040, abstract = {Formation during the first cycles of Li-rich layered oxide (LRLO) cathode materials consolidates the interphase and leads to structural changes that are decisive for long-term cyclability. However, the nature and effect of the changes are material-dependent and unknown for the important class of Co-free, Ni-poor LRLOs. Here, we analyze the processes during the tailored formation procedure of a typical class member, Li1.28Ni0.15Mn0.57O2, and demonstrate that it remarkably changes lattice composition and structure as a prerequisite for stable cycling. We combine electrochemistry, operando mass spectrometry, X-ray diffraction, and X-ray absorption spectroscopy with density functional theory simulations. Activation most prominently compresses the layer spacing along the c-axis and increases reversible structural breathing. The large capacity of ∼250 mAh g–1 originates from the Ni2+/Ni4+ and O2–/O– redox couples. Electron exchange during O-redox is smeared over the entire anionic sublattice rather than localized on specific oxygen atomic sites. This redox mechanism is reversible without detrimental oxygen evolution, avoiding continued degradation common in conventional LRLOs. Sequential Ni- and O-redox during activation irreversibly distorts the coordination of the redox-inactive Mn4+ centers. This structural evolution of the MnO6 octahedra appears to enable the superior electrochemical performance of this LRLO phase. These findings define an activation pathway for the important class of Co-free, Ni-poor LRLOs, offering potential guidance for the rational design of high-performance, more sustainable cathode materials.}, author = {Busato, Matteo and Tuccillo, Mariarosaria and Celeste, Arcangelo and Tofoni, Alessandro and Silvestri, Laura and D’Angelo, Paola and Freunberger, Stefan Alexander and Brutti, Sergio}, issn = {2574-0962}, journal = {ACS Applied Energy Materials}, number = {1}, pages = {686--697}, publisher = {American Chemical Society}, title = {{Structural rearrangements of a Cobalt-free Lithium-rich layered oxide cathode during formation}}, doi = {10.1021/acsaem.5c03511}, volume = {9}, 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}, } @misc{21284, abstract = {The advantageous characteristics attributed to the 19F nucleus have made it a popular target for NMR once again in recent years. Aside from solution NMR, an increasing number of studies have been conducted applying solid-state magic-angle-spinning NMR to fluorine-labeled samples. Here, the high chemical shift anisotropy and strong dipolar couplings can be utilized to get structural insights into proteins and measure long distances. Despite increasing popularity and promising benefits, the sensitivity of biomolecular 19F MAS NMR often suffers from slow longitudinal T1 relaxation and therefore long recycle delays. In this work, we expand paramagnetic doping, an approach commonly used to reduce proton T1 relaxation times, to 19F-labeled biological samples. We study the effect of Gd(DTPA) and Gd(DTPA-BMA) on 19F and 13C T1 and T2 relaxation in a [5-19F13C]-tryptophan-labeled protein via 19F-detected MAS NMR experiments. The observed paramagnetic relaxation enhancement substantially reduces measurement times of 19F MAS NMR experiments without compromising resolution. Additionally, we report the chemical-shift assignments of all four fluorotryptophan signals in the 12 × 39 kDa large protein using a mutagenesis approach.}, author = {Becker, Lea Marie and Schanda, Paul}, publisher = {Institute of Science and Technology Austria}, title = {{Research data for "Accelerated 19F biomolecular magic-angle spinning NMR with paramagnetic dopants"}}, doi = {10.15479/AT-ISTA-21284}, year = {2026}, } @article{21485, abstract = {Insulating oxides are among the most abundant solid materials in the universe1,2,3. Of the many ways in which they influence natural phenomena, perhaps the most consequential is their capacity to transfer electrical charge during contact4,5,6,7,8,9,10—which occurs even between samples of the same oxide—yet the symmetry-breaking parameter that causes this remains unidentified11,12. Here we show that adventitious carbonaceous molecules adsorbed from the environment are the symmetry-breaking factor in same-material oxide contact electrification (CE). We use acoustic levitation to measure charge exchange between a sphere and a plate composed of identical amorphous silicon dioxide (SiO2). Although charging polarity is random for co-prepared samples, we control it with baking or plasma treatment. Observing the charge-exchange relaxation afterwards, we see dynamics over a timescale of hours and connect this directly to the presence of adventitious carbon with time-of-flight mass spectrometry, low-energy ion scattering and infrared spectroscopy. Going further, we confirm that adventitious carbon can even determine charge exchange among different oxides. Our results identify the symmetry-breaking parameter that causes insulating oxides to exchange charge in settings ranging from desert sands4 to volcanic plumes5,6, while simultaneously highlighting an overlooked factor in CE more broadly.}, author = {Grosjean, Galien M and Ostermann, Markus and Sauer, Markus and Hahn, Michael and Pichler, Christian M. and Fahrnberger, Florian and Pertl, Felix and Balazs, Daniel and Link, Mason M. and Kim, Seong H. and Schrader, Devin L. and Blanco, Adriana and Gracia, Francisco and Mujica, Nicolás and Waitukaitis, Scott R}, issn = {1476-4687}, journal = {Nature}, number = {8106}, pages = {626--631}, publisher = {Springer Nature}, title = {{Adventitious carbon breaks symmetry in oxide contact electrification}}, doi = {10.1038/s41586-025-10088-w}, volume = {651}, 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{21750, abstract = {Liquid-like superionic conductors, with highly mobile ions in a rigid framework, offer intrinsically low lattice thermal conductivity without compromising electronic transport. Argyrodite-type Ag8SnSe6 exhibits a melt-like Ag sublattice that drives lattice thermal conductivity (κL) below 0.2 watts per meter per kelvin, yet its low carrier concentration limits the power factor. Here, interstitial Ag atoms raise the Fermi level into the conduction band, substantially increasing the electron concentration. Simultaneously, the formation of a secondary Ag2Se phase generates lattice distortions that enhance phonon scattering. A pronounced mismatch between electronic (~200 nanometers) and phononic (~0.22 nanometers) mean free paths decouples charge and heat transport, enabling concurrent suppression of κL and retention of high electrical conductivity. This coupled electronic-phononic modulation yields a record ZT of 0.72 at ambient temperature and a peak ZT of 1.1 at 735 kelvins, with an average ZTavg of 0.72 over 320 to 735 kelvins. A unicouple device achieves 6.3% efficiency under a 357-kelvin gradient, highlighting a practical strategy for high-performance midtemperature thermoelectrics.}, author = {Li, Mengyao and Zhao, Xueke and Zhang, Yu and Yu, Jing and Liu, Xuyang and Jia, Mochen and Song, Hongzhang and Wang, Dongyang and Arbiol, Jordi and Ibáñez, Maria and Shan, Chongxin and Cabot, Andreu and Wang, Ziyu}, issn = {2375-2548}, journal = {Science Advances}, number = {15}, publisher = {AAAS}, title = {{Electronic-phononic decoupling and Fermi-level tuning enable high thermoelectric performance in Ag8SnSe6}}, doi = {10.1126/sciadv.aec9073}, volume = {12}, 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}, } @article{21776, abstract = {Pyridyl motifs equipped with N-substituents can be powerful ligands for catalysis, yet their broader adoption is limited by the lack of a practical method to prepare these scaffolds. We report a modular, robust, and versatile Buchwald–Hartwig amination protocol that enables the rapid synthesis of bipyridine, phenanthroline, terpyridine, and pybox ligands bearing dialkylamine, diarylamine, and heteroaromatic N-substituents. These conditions streamline ligand library synthesis and will facilitate systematic studies in catalysis and related applications.}, author = {Petrik, Adam and Bena, Aleksander and Baunis, Haralds and Kelch, Riley M. and Yoon, Tehshik P. and Pieber, Bartholomäus}, issn = {1615-4169}, journal = {Advanced Synthesis & Catalysis}, number = {9}, publisher = {Wiley}, title = {{Facile access to N-substituted pyridyl ligands}}, doi = {10.1002/adsc.70417}, volume = {368}, year = {2026}, } @article{21914, abstract = {Cyclic adenosine monophosphate (cAMP) is a fundamental second messenger involved in diverse signaling pathways across both animals and plants. While the role of 3′,5′-cAMP has been extensively characterized, the biological significance of its structural isomer, 2′,3′-cAMP, remains largely unexplored, particularly in plants. Here, we show that 2′,3′-cAMP and 3′,5′-cAMP represent parallel signaling systems in Arabidopsis thaliana, with different enzymatic origins and largely distinct downstream effects. In vitro enzymatic assays show that plant adenylate cyclases (ACs), including AFB5 and HpAC1, produce specifically 3′,5′-cAMP from ATP, whereas the TIR domain of protein L7 also catalyzes the formation of 2′,3′-cAMP from RNA. Comprehensive multiomics analyses reveal that two isomers elicit distinct yet partially overlapping metabolic, proteomic, and transcriptional response: 2′,3′-cAMP activates broad, stress-adaptive gene expression reprogramming, while 3′,5′-cAMP fine-tunes responses related to nutrient status and cellular homeostasis. Our findings establish the existence of dual cAMP signaling systems in plants, each with specialized functions and provide insights into the complex regulatory networks governing plant physiology.}, author = {Li, Mingyue and Chodasiewicz, Monika and Muraleedharan, Malavika and Lopez, Israel M. and Gorka, Michal and Kerber, Olga and Alotaibi, Saqer S. and Nelson, Andrew D.L. and Lenobel, Rene and Friedecká, Jaroslava and Skirycz, Aleksandra and Friml, Jiří}, issn = {2375-2548}, journal = {Science Advances}, number = {19}, publisher = {AAAS}, title = {{Biogenesis and downstream effects of 3',5' and 2',3' cAMP isomers in plants}}, doi = {10.1126/sciadv.aea7828}, volume = {12}, 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}, } @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{22333, abstract = {RNA polymerase II (Pol II) must be assembled in the cytoplasm before it enters the nucleus, where it transcribes protein-coding genes. Although transcription by Pol II is intensively studied, how this central multi-subunit enzyme is made and the role of dedicated assembly factors remains unclear. Here, we report the integrative structural analysis of a native human Pol II from the cytoplasm captured near the end of biogenesis. The complex contains Gdown1 and three biogenesis factors – RPAP2 and the critical small GTPases GPN1 and GPN3. Cryo-EM analysis of the complex reveals how Gdown1 and RPAP2 associate with Pol II and prevent the premature association of transcription factors. Further biochemical and cryo-EM analysis reveals how RPAP2 tethers GPN1–GPN3 to the complex and how the assembly of the RPAP2–GPN1–GPN3 complex is controlled by GTP hydrolysis. The combined results uncover a network of interactions that chaperone cytoplasmic Pol II to prevent aberrant interactions, reveal a molecular switch regulating biogenesis factor association, and suggest a general mechanism for the action of GPN-loop GTPase family of enzymes.}, author = {Hlavata, Annamaria and Neuditschko, Benjamin and Schellhaas, Ulla and Plaschka, Clemens and Herzog, Franz and Bernecky, Carrie A}, issn = {2041-1723}, journal = {Nature Communications}, publisher = {Springer Nature}, title = {{Structure of cytoplasmic RNA polymerase II}}, doi = {10.1038/s41467-026-75416-8}, year = {2026}, } @article{21777, abstract = {The advantageous characteristics attributed to the 19F nucleus have made it a popular target for nuclear magnetic resonance (NMR) once again in recent years. Aside from solution NMR, an increasing number of studies have been conducted applying solid-state magic-angle spinning (MAS) NMR to fluorine-labelled samples. Here, the high chemical shift anisotropy and strong dipolar couplings can be utilised to get structural insights into proteins and measure long distances. Despite increasing popularity and promising benefits, the sensitivity of biomolecular 19F MAS NMR often suffers from slow longitudinal T1 relaxation and therefore long recycle delays. In this work, we expand paramagnetic doping, an approach commonly used to reduce proton T1 relaxation times, to 19F-labelled biological samples. We study the effect of Gd(DTPA) and Gd(DTPA-BMA) on 19F T1 and T2, and 13C T1 and T2 relaxation in a [5-19F13C]-tryptophan-labelled protein via 19F-detected MAS NMR experiments. The observed paramagnetic relaxation enhancement substantially reduces measurement times of 19F MAS NMR experiments without compromising resolution. Additionally, we report the chemical shift assignments of all four fluorotryptophan signals in the 12×39 kDa-large protein TET2 using a mutagenesis approach.}, author = {Becker, Lea Marie and Toscano, Giorgia and Kapitonova, Anna and Singh, Rajkumar and Guillerm, Undina and Lichtenecker, Roman J. and Schanda, Paul}, issn = {2699-0016}, journal = {Magnetic Resonance}, number = {1}, pages = {29--37}, publisher = {Copernicus Publications}, title = {{Accelerated 19F biomolecular magic-angle spinning NMR with paramagnetic dopants}}, doi = {10.5194/mr-7-29-2026}, volume = {7}, 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{21730, abstract = {Hydrogen peroxide (H2O2) is a crucial member of the reactive oxygen species (ROS) family, playing roles in cellular signalling and immune responses in human health. Moreover, it is a potential biomarker of diabetes when present in aberrant concentrations. Therefore, monitoring trace levels of H2O2 has become a research hotspot for analytical and sensor chemists. In this context, we report a rhodamine-based fluorescent probe (RN), which shows excellent fluorescent enhancement at 555 nm upon the addition of H2O2 along with a low limit of detection (LOD) of 0.67 ppm and fast response (∼2 min). The probe is highly selective for H2O2, showing no fluorescence enhancement with other ROS. RN is synthesised in a one-pot chemical reaction using rhodamine 6G (R6G) and 4,7,10-trioxa-1,13-tridecanediamine (TTDA). H2O2 detection in pre-treated milk samples proves its real-world viability. We found that RN shows low cytotoxicity, which allowed us to successfully explore its potential to monitor H2O2 generation in a diabetic L929 skin cell line and diabetic mice liver tissue. This result demonstrates promising features for assessing early diabetic progression through fluorescence imaging.}, author = {Mondal, Moumita and Ghorai, Pravat and Samadder, Asmita and Freunberger, Stefan Alexander and Banerjee, Priyabrata}, issn = {2050-7518}, journal = {Journal of Materials Chemistry B}, number = {17}, pages = {5314--5322}, publisher = {Royal Society of Chemistry}, title = {{H2O2 responsive rhodamine-based probe for monitoring early-stage diabetes diagnosis}}, doi = {10.1039/d5tb02687c}, volume = {14}, 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}, } @article{22608, abstract = {For tissues to spread, they must deform while staying intact. How spreading tissues balance flexibility with integrity is not yet well understood. Here, we show that keratin intermediate filaments adapt tissue mechanical resilience to the stresses arising in epithelial tissues during spreading. By analyzing the expansion of the enveloping cell layer (EVL) over the yolk cell in zebrafish embryos in vivo, we find 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, to prevent tissue rupture. Further, keratins are required in the yolk cell for mechanosensitive actomyosin network contraction and flow, the forces pulling the EVL. These dual mechanosensitive functions of keratins enable a balance between pulling force production and EVL mechanical resilience, 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}, issn = {2041-1723}, journal = {Nature Communications}, publisher = {Springer Nature}, title = {{Keratins coordinate tissue spreading by balancing spreading forces with tissue material properties}}, doi = {10.1038/s41467-026-72366-z}, volume = {17}, year = {2026}, }