@article{20048, abstract = {During embryonic development, cell behaviors need to be tightly regulated in time and space. Yet how the temporal and spatial regulations of cell behaviors are interconnected during embryonic development remains elusive. To address this, we turned to zebrafish gastrulation, the process whereby dynamic cell behaviors generate the three principal germ layers of the early embryo. Here, we show that Hoxb cluster genes are expressed in a temporally collinear manner at the blastoderm margin, where mesodermal and endodermal (mesendoderm) progenitor cells are specified and ingress to form mesendoderm/hypoblast. Functional analysis shows that these Hoxb genes regulate the timing of cell ingression: under- or overexpression of Hoxb genes perturb the timing of mesendoderm cell ingression and, consequently, the positioning of these cells along the forming anterior-posterior body axis after gastrulation. Finally, we found that Hoxb genes control the timing of mesendoderm ingression by regulating cellular bleb formation and cell surface fluctuations in the ingressing cells. Collectively, our findings suggest that Hoxb genes interconnect the temporal and spatial pattern of cell behaviors during zebrafish gastrulation by controlling cell surface fluctuations.}, author = {Moriyama, Yuuta and Mitsui, Toshiyuki and Heisenberg, Carl-Philipp J}, issn = {1477-9129}, journal = {Development}, number = {12}, publisher = {The Company of Biologists}, title = {{Hoxb genes determine the timing of cell ingression by regulating cell surface fluctuations during zebrafish gastrulation}}, doi = {10.1242/dev.204261}, volume = {152}, year = {2025}, } @article{20050, abstract = {We prove upper bounds on the L∞-Wasserstein distance from optimal transport between strongly log-concave probability densities and log-Lipschitz perturbations. In the simplest setting, such a bound amounts to a transport-information inequality involving the L∞-Wasserstein metric and the relative L∞-Fisher information. We show that this inequality can be sharpened significantly in situations where the involved densities are anisotropic. Our proof is based on probabilistic techniques using Langevin dynamics. As an application of these results, we obtain sharp exponential rates of convergence in Fisher’s infinitesimal model from quantitative genetics, generalising recent results by Calvez, Poyato, and Santambrogio in dimension 1 to arbitrary dimensions.}, author = {Khudiakova, Kseniia and Maas, Jan and Pedrotti, Francesco}, issn = {1050-5164}, journal = {The Annals of Applied Probability}, number = {3}, pages = {1913--1940}, publisher = {Institute of Mathematical Statistics}, title = {{L∞-optimal transport of anisotropic log-concave measures and exponential convergence in Fisher’s infinitesimal model}}, doi = {10.1214/25-aap2162}, volume = {35}, year = {2025}, } @inproceedings{20052, abstract = {This paper revisits a fundamental distributed computing problem in the population protocol model. Provided n agents each starting with an input color in [k], the relative majority problem asks to find the predominant color. In the population protocol model, at each time step, a scheduler selects two agents that first learn each other's states and then update their states based on what they learned. We present the Circles protocol that solves the relative majority problem with k3 states. It is always-correct under weakly fair scheduling. Not only does it improve upon the best known upper bound of O(k7), but it also shows a strikingly simpler design inspired by energy minimization in chemical settings.}, author = {Breitkopf, Tom-Lukas and Dallot, Julien and El-Hayek, Antoine and Schmid, Stefan}, booktitle = {Proceedings of the ACM Symposium on Principles of Distributed Computing}, isbn = {9798400718854}, location = {Huatulco, Mexico}, pages = {549--552}, publisher = {Association for Computing Machinery}, title = {{Brief announcement: Minimizing energy solves relative majority with a cubic number of states in population protocols}}, doi = {10.1145/3732772.3733512}, year = {2025}, } @inproceedings{20053, abstract = {Liquid democracy is a transitive vote delegation mechanism over voting graphs. It enables each voter to delegate their vote(s) to another better-informed voter, with the goal of collectively making a better decision. The question of whether liquid democracy outperforms direct voting has been previously studied in the context of local delegation mechanisms (where voters can only delegate to someone in their neighbourhood) and binary decision problems. It has previously been shown that it is impossible for local delegation mechanisms to outperform direct voting in general graphs. This raises the question: for which classes of graphs do local delegation mechanisms yield good results? In this work, we analyse (1) properties of specific graphs and (2) properties of local delegation mechanisms on these graphs, determining where local delegation actually outperforms direct voting. We show that a critical graph property enabling liquid democracy is that the voting outcome of local delegation mechanisms preserves a sufficient amount of variance, thereby avoiding situations where delegation falls behind direct voting1. These insights allow us to prove our main results, namely that there exist local delegation mechanisms that perform no worse and in fact quantitatively better than direct voting in natural graph topologies like complete, random d-regular, and bounded degree graphs, lending a more nuanced perspective to previous impossibility results.}, author = {Chatterjee, Krishnendu and Gilbert, Seth and Schmid, Stefan and Svoboda, Jakub and Yeo, Michelle X}, booktitle = {Proceedings of the ACM Symposium on Principles of Distributed Computing}, isbn = {9798400718854}, location = {Huatulco, Mexico}, pages = {241--251}, publisher = {Association for Computing Machinery}, title = {{When is liquid democracy possible?: On the manipulation of variance}}, doi = {10.1145/3732772.3733544}, year = {2025}, } @inproceedings{20055, abstract = {Supercrystals represent three-dimensional orderings of colloidal nanocrystals (NCs), showcasing collective properties in photonics, phononics, and electronics applications.1,2 Recent studies have shown that such assemblies are directly produced during nanocrystal reactions.3–6 However, a fundamental understanding of in situ formed supercrystals that withstand typical NC purification processes remains underexplored, which is important for further use. Herein, we report the reaction precursor-mediated formation of stable PbTe supercrystals. Rationalizing the formation of these assemblies through small-angle x-ray scattering (SAXS) measurements, we unveil their formation mechanism. Our findings reveal that the supercrystal formation occurs in the presence of an excess of lead oleates in the crude solution. It should be noted that the formed supercrystals can be stabilized under specific conditions determined by the lead oleate cluster concentration, content of trioctylphosphine telluride (TOP-Te), NC size and the need of an annealing step at mild conditions. Furthermore, this approach allows for the continuous growth of a secondary phase within the supercrystal; for example in the case of PbTe supercrystals, a PbS shell can be grown on each PbTe NC constituent, resulting in core-shell PbTe-PbS supercrystals. Our work elucidates that reaction precursors play an important role in in situ SC formation and stabilization, implying the possibility of applying this knowledge to other NC reactions.}, author = {Lee, Seungho and Balazs, Daniel and Horta, Sharona and Rayaroth Puthiyaveettil, Aiswarya and Ibáñez, Maria}, booktitle = {Proceedings of the MATSUS Spring 2025 Conference}, location = {Sevilla, Spain}, publisher = {Fundació de la comunitat valenciana SCITO}, title = {{Reaction precursor-mediated formation of stable supercrystals in colloidal nanocrystal synthesis: PbTe case}}, doi = {10.29363/nanoge.matsusspring.2025.173}, year = {2025}, } @article{20056, abstract = {Theoretical studies have shown that stochasticity can affect the dynamics of ecosystems in counterintuitive ways. However, without knowing the equations governing the dynamics of populations or ecosystems, it is difficult to ascertain the role of stochasticity in real datasets. Therefore, the inverse problem of inferring the governing stochastic equations from datasets is important. Here, we present an equation discovery methodology that takes time series data of state variables as input and outputs a stochastic differential equation. We achieve this by combining traditional approaches from stochastic calculus with the equation discovery techniques. We demonstrate the generality of the method via several applications. First, we deliberately choose various stochastic models with fundamentally different governing equations, yet they produce nearly identical steady-state distributions. We show that we can recover the correct underlying equations, and thus infer the structure of their stability, accurately from the analysis of time series data alone. We demonstrate our method on two real-world datasets—fish schooling and single-cell migration—that have vastly different spatiotemporal scales and dynamics. We illustrate various limitations and potential pitfalls of the method and how to overcome them via diagnostic measures. Finally, we provide our open-source code via a package named PyDaDDy (Python Library for Data-Driven Dynamics).}, author = {Nabeel, Arshed and Karichannavar, Ashwin and Palathingal, Shuaib and Jhawar, Jitesh and Brückner, David and Raj M, Danny and Guttal, Vishwesha}, issn = {1537-5323}, journal = {The American Naturalist}, number = {4}, pages = {E100--E117}, publisher = {University of Chicago Press}, title = {{Discovering stochastic dynamical equations from ecological time series data}}, doi = {10.1086/734083}, volume = {205}, year = {2025}, } @phdthesis{20074, abstract = {Prenatal immune challenges pose significant risks to human embryonic brain and eye development. However, we still lack knowledge about the safe usage of anti-inflammatory drugs during pregnancy. Human induced pluripotent stem cell (hIPSC)-derived brain organoid models provide a unique opportunity to investigate neuronal development and have started to explore functional consequences upon viral infection. However, brain organoids usually lack microglia, the brain-resident immune cells. They are present in the early human embryonic brain and actively participate in neuronal circuit development. At the same time, microglia are known for their immune-sensing properties and will influence viral-mediated effects. In my thesis, I was interested to study the multifunctional role of human microglia during retinal development. In chapter 1, I characterize the innate occurrence of IBA1+-microglia-like cells within the retinal organoid differentiation (Bartalska et al., 2022). Therefore, we differentiate hIPSC using an unguided retinal organoid differentiation protocol and observe the presence of IBA1+-microglia-like cells alongside retinal cups between week 3 and 4 in 2.5D culture. However, instead of infiltrating the neuroectodermal sides, they enrich within non-pigmented, 3D-cystic compartments that develop in low numbers parallel to 3D-retinal organoids. To enrich for IBA1+-microglia precursors (preMG), we guided the differentiation with a low-dosed BMP4 application, which prevents retinal cup development and enhances microglia and 3D-cysts formation. We characterize the differentiated preMG for their microglia-like identity and validated their functionality. In parallel, mass spectrometry identifies the 3D-cysts to express mesenchymal and epithelial markers. We confirm that comparable 3D-cysts are also the preferential environment for IBA1+-microglia-like cells within the unguided retinal organoid differentiation. In chapter 2, I investigate how microglia influence retinal development and whether they contribute to viral-mediated consequences (Schmied et al., 2025). Here, we assemble preMG, which we have characterized in chapter 1, into 3D-retinal organoids. Once the outer plexiform layer forms, microglia-like cells (iMG) populate them and interact with retinal cell types. However, at this developmental stage, the ganglion cell number decreases in 3D-retinal organoids. Thus, we adapted the model into 2D which promotes their survival. Integrated iMG engulf ganglion cells and control their cell number. In parallel, we apply the immunostimulant POLY(I:C) to mimic a fetal viral infection. Although POLY(I:C) stimulation affects iMG phenotype, it does not influence their interaction with ganglion cells. Furthermore, iMG presence significantly contributes to the supernatant’s inflammatory secretome and increases retinal cell proliferation. Simultaneous exposure to the non-steroidal anti-inflammatory drug (NSAID) ibuprofen dampens POLY(I:C)-mediated consequences of the iMG phenotype and ameliorates cell proliferation. Remarkably, while POLY(I:C) disrupts neuronal calcium dynamics independent of iMG presence, ibuprofen rescues this effect only in the presence of iMG. Mechanistically, ibuprofen blocks the enzymes cyclooxygenase 1 and 2 (COX1/ PTGS1 and COX2/ PTGS2) simultaneously, from which iMG predominantly express COX1. Selective inhibition of COX1 does not restore the calcium peak amplitude upon POLY(I:C) stimulation, indicating ibuprofen’s effect depends on the presence and interplay of both, COX1 and COX2. In summary, we characterized the 3D-retinal organoid model for the occurrence of IBA1+-microglia like cells. As the innately developing IBA1+-cells enrich in mesenchymal over retinal structures, we optimized a protocol to differentiate IBA1+-microglia precursors. By combining these two models we generate microglia-assembled retinal organoids. Our results underscore the importance of microglia during neurodevelopment, in the context of prenatal immune challenges and provide insight into the mechanisms by which ibuprofen exerts its protective effects during embryonic development.}, author = {Hübschmann, Verena}, isbn = {978-3-99078-060-2}, issn = {2663-337X}, pages = {151}, publisher = {Institute of Science and Technology Austria}, title = {{ Human microglia impact neuronal development in retinal organoids}}, doi = {10.15479/AT-ISTA-20074}, year = {2025}, } @article{20077, abstract = {Hyaluronic acid (HA) is a key extracellular matrix component of vertebrates, where it mediates cell adhesion, immune regulation, and tissue remodeling through its interaction with specific receptors. Although HA has been detected in a few invertebrate species, the lack of fundamental components of the molecular HA pathway poses relevant objections about its functional role in these species. Mining genomic and transcriptomic data, we considered the conservation of the gene locus encoding for the extracellular link protein (XLINK) in marine mussels as well as its expression patterns. Structural and phylogenetic analyses were undertaken to evaluate possible similarities with vertebrate orthologs and to infer the origin of this gene in invertebrates. Biochemical analysis was used to quantify HA in tissues of Mytilus galloprovincialis. As a result, we confirm that the mussel can produce HA (up to 1.02 ng/mg in mantle) and that its genome encodes two XLINK gene loci. These loci are conserved in Mytilidae species and show a complex evolutionary path. Mussel XLINK genes appeared to be expressed during developmental stages in three mussel species, ranking in the top 100 expressed genes in M. trossulus at 17 h post-fertilization. In conclusion, the presence of HA and an active gene with the potential to bind HA suggests that mussels have the potential to synthesize and use HA and are among the few invertebrates encoding this gene.}, author = {Rosani, Umberto and Altan, Nehir and Venier, Paola and Bortoletto, Enrico and Volpi, Nicola and Bernecky, Carrie A}, issn = {2079-7737}, journal = {Biology}, number = {8}, publisher = {MDPI}, title = {{Ancestral origin and functional expression of a hyaluronic acid pathway complement in mussels}}, doi = {10.3390/biology14080930}, volume = {14}, year = {2025}, } @article{20079, abstract = {Research question: Is LINC01638 involved in regulation of epithelial-to-mesenchymal transition (EMT) in endometriosis? Design: A prospective patient cohort study was combined with functional experiments in the 12Z endometriosis epithelial cell line to investigate the role of LINC01638 in endometriosis. Eutopic endometrial samples were collected by curettage, and ectopic endometrial lesion samples were collected by laparoscopic surgery from 24 control patients and 41 patients with endometriosis. The phenotype of 12Z cells was assessed following LINC01638 knockdown using siRNA, performing proliferation, adhesion, migration and invasion assays, as well as assessing apoptosis and cell cycle changes with flow cytometry assays. In order to assess the relationship between LINC01638 and histone deacetylase class 1 enzyme (HDAC1), LINC01638 knockdown was combined with HDAC inhibition with the specific HDAC inhibitor romidepsin. Results: LINC01638 was up-regulated in the epithelial layer of endometriotic lesions, and LINC01638 knockdown in 12Z cells led to reduced proliferation, adhesion, migration and invasion. The reduction in proliferation was associated with increased p21 and p27 expression, and G1 phase arrest. Further analysis of LINC01638 control and knockdown cells revealed that a number of transcription factors associated with EMT are down-regulated in knockdown cells, along with the cytoskeleton regulatory gene RHOB, while HDAC1 was up-regulated. Chromatin immunoprecipitation analysis and HDAC1 inhibitory treatment combined with LINC01638 knockdown indicated that LINC01638 regulates RHOB expression via HDAC1-mediated promoter deacetylation. RHOB is up-regulated in the epithelial layer of endometriotic lesions compared with eutopic endometrium, supporting a role in the disease. Conclusions: LINC01638 is an epigenetic regulator of the pathogenesis of endometriosis, promoting proliferation and EMT of endometriotic lesions.}, author = {Yotova, Iveta and Proestling, Katharina and Pauler, Florian and Rainer, Lisa and Kaup, Leonie and Heine, Jana and Sandrieser, Lejla and Wenzl, René and Hudson, Quanah J.}, issn = {1472-6491}, journal = {Reproductive Biomedicine Online}, number = {3}, publisher = {Elsevier}, title = {{LINC01638 promotes epithelial-to-mesenchymal transition in endometriosis epithelial cells by up-regulating RHOB via HDAC1 suppression}}, doi = {10.1016/j.rbmo.2025.104942}, volume = {51}, year = {2025}, } @article{20080, abstract = {Introduction: Acid-growth theory has been postulated in the 70s to explain the rapid elongation of plant cells in response to the hormone auxin. More recently, it has been demonstrated that activation of the proton ATPs pump (H+-ATPs) promoting acidification of the apoplast is the principal mechanism by which auxin and other hormones such as brassinosteroids (BR) induce cell elongation. Despite these advances, the impact of this acidification on the mechanical properties of the cell wall remained largely unexplored. Methods: Here, we use elongation assays of Arabidopsis thaliana hypocotyls and Atomic Force Microscopy (AFM) to correlate hormone-induced tissue elongation and local changes in cell wall mechanical properties. Furthermore, employing transgenic lines over-expressing Pectin Methyl Esterase (PME), along with calcium chelators, we investigate the effect of pectin modification in hormone-driven cell elongation. Results: We demonstrate that acidification of apoplast is necessary and sufficient to induce cell elongation through promoting cell wall softening. Moreover, we show that enhanced PME activity can induce both cell wall softening or stiffening in extracellular calcium dependent-manner and that tight control of PME activity is required for proper hypocotyl elongation. Discussion: Our results confirm a dual role of PME in plant cell elongation. However, further investigation is needed to assess the status of pectin following short- or long-term PME treatments in order to determine if pectin methyl-esterification might promote its degradation as well as the role of PME inhibitors upon PME induction.}, author = {Gallemi, Marçal and Montesinos López, Juan C and Zarevski, Nikola and Pribyl, Jan and Skládal, Petr and Hannezo, Edouard B and Benková, Eva}, issn = {1664-462X}, journal = {Frontiers in Plant Science}, publisher = {Frontiers Media}, title = {{Dual role of pectin methyl esterase activity in the regulation of plant cell wall biophysical properties}}, doi = {10.3389/fpls.2025.1612366}, volume = {16}, year = {2025}, } @article{20082, abstract = {Efficient immune responses rely on the capacity of leukocytes to traverse diverse and complex tissues. To meet such changing environmental conditions, leukocytes usually adopt an ameboid configuration, using their forward-positioned nucleus as a probe to identify and follow the path of least resistance among pre-existing pores. We show that, in dense environments where even the largest pores preclude free passage, leukocytes position their nucleus behind the centrosome and organelles. The local compression imposed on the cell body by its surroundings triggers assembly of a central F-actin pool, located between cell front and nucleus. Central actin pushes outward to transiently dilate a path for organelles and nucleus. Pools of central and front actin are tightly coupled and experimental depletion of the central pool enhances actin accumulation and protrusion formation at the cell front. Although this shifted balance speeds up cells in permissive environments, migration in restrictive environments is impaired, as the unleashed leading edge dissociates from the trapped cell body. Our findings establish an actin regulatory loop that balances path dilation with advancement of the leading edge to maintain cellular coherence.}, author = {Dos Reis Rodrigues, Patricia and Avellaneda Sarrió, Mario and Canigova, Nikola and Gärtner, Florian R and Vaahtomeri, Kari and Riedl, Michael and De Vries, Ingrid and Merrin, Jack and Hauschild, Robert and Fukui, Yoshinori and Juanes Garcia, Alba and Sixt, Michael K}, issn = {1529-2916}, journal = {Nature Immunology}, pages = {1258–1266}, publisher = {Springer Nature}, title = {{Migrating immune cells globally coordinate protrusive forces}}, doi = {10.1038/s41590-025-02211-w}, volume = {26}, year = {2025}, } @article{20098, abstract = {Climate change is causing wildfires to become more frequent and intense. While predicting burned areas using bioclimatic and anthropogenic factors is an active research area, few studies have examined what drives the economic damages of wildfires. Our study aims to fill this gap by analyzing key factors influencing global economic wildfire damages and projecting future damages under three shared socioeconomic pathways (SSPs). We apply regression analyses to identify significant predictors of economic wildfire damages at country levels and use the fitted model to project future damages under SSP126, SSP245, and SSP370. Results show that the human vulnerability index (HVI), reflecting socioeconomic conditions, is the strongest predictor of historical wildfire damages, followed by water vapor pressure deficit during the fire season and population density around forested areas. We found high population density to be associated with lower damages. These findings contrast with studies of burned areas, where climate factors are more dominant. Our model projects that by 2070, average global economic wildfire damages will be three times higher under SSP370 than SSP126. Our model also shows that following SSP126 not only reduces wildfire damages but also lessens the inequalities in damage distribution across countries. This pathway’s dual focus on equitable socioeconomic progress and climate action potentially enhances a country’s resilience that helps mitigate wildfire damages. Our analyses also indicate that strong socioeconomic development can offset wildfire damages associated with climate hazards, although this is less certain under SSP370. SSP126’s integrated approach improves both socioeconomic conditions and limits global warming, providing substantial benefits to less developed countries while still reducing damages in developed nations, despite their already low HVI scores. Our work complements existing research on burned areas and underscores the importance of sustainable development and international collaboration in reducing the economic damages of wildfires.}, author = {Hwong, Yi-Ling and Byers, Edward and Werning, Michaela and Quilcaille, Yann}, issn = {2752-5295}, journal = {Environmental Research: Climate}, number = {3}, publisher = {IOP Publishing}, title = {{Sustainable development key to limiting climate change-driven wildfire damages}}, doi = {10.1088/2752-5295/adec11}, volume = {4}, year = {2025}, } @article{20099, abstract = {The hippocampus, critical for learning and memory, is dogmatically described as a trisynaptic circuit where dentate gyrus granule cells (GCs), CA3 pyramidal neurons (PNs), and CA1 PNs are serially connected. However, CA3 also forms an autoassociative network, and its PNs have diverse morphologies, intrinsic properties, and GC input levels. How PN subtypes compose this recurrent network is unknown. To determine the synaptic arrangement of identified CA3 PNs, we combine multicellular patch-clamp recording and post hoc morphological analysis in mouse hippocampal slices. PNs can be divided into distinct “superficial” and “deep” subclasses, the latter including previously reported “athorny” cells. Subclasses have distinct input-output transformations and asymmetric connectivity, which is more abundant from superficial to deep PNs, splitting CA3 locally into two parallel recurrent networks. Coincident spontaneous inhibition occurs frequently within but not between subclasses, implying subclass-specific inhibitory innervation. Our results suggest two separately controlled sublayers for parallel information processing in hippocampal CA3.}, author = {Watson, Jake and Vargas Barroso, Victor M and Jonas, Peter M}, issn = {2211-1247}, journal = {Cell Reports}, number = {8}, publisher = {Elsevier}, title = {{Cell-specific wiring routes information flow through hippocampal CA3}}, doi = {10.1016/j.celrep.2025.116080}, volume = {44}, year = {2025}, } @article{20100, abstract = {A key step in protein structure prediction involves the detection of co-evolving pairs of residues, a signal for spatial proximity. This information is gleaned from multiple sequence alignment and underscores Alphafold’s structure prediction for almost every known protein. A simple means to create proteins beyond those found in nature, is by unnaturally fusing together two known proteins or protein parts. Here we demonstrate that structured peptides are predicted with significantly reduced accuracy when added to the terminal ends of scaffold proteins. Appending the multiple sequence alignment for the individual peptide tags to that of the scaffold protein often restores prediction accuracy. This work suggests that this windowed multiple sequence alignment approach can be a useful tool for predicting the structure of fused, chimeric proteins.}, author = {Vedula, Sanketh and Bronstein, Alexander and Marx, Ailie}, issn = {2001-0370}, journal = {Computational and Structural Biotechnology Journal}, pages = {3292--3298}, publisher = {Elsevier}, title = {{Improving prediction accuracy in chimeric proteins with windowed multiple sequence alignment}}, doi = {10.1016/j.csbj.2025.07.039}, volume = {27}, year = {2025}, } @article{20102, abstract = {Speciation is rarely observable directly. A way forward is to compare pairs of ecotypes that evolved in parallel in similar contexts but have reached different degrees of reproductive isolation. Such comparisons are possible in the marine snail Littorina saxatilis by contrasting barriers to gene flow between parallel ecotypes in Spain and Sweden. In both countries, divergent ecotypes have evolved to withstand either crab predation or wave action. Here, we explore transects spanning contact zones between the Crab and the Wave ecotypes using low-coverage whole-genome sequencing, morphological and behavioural traits. Despite parallel phenotypic divergence, distinct patterns of differentiation between the ecotypes emerged: a continuous cline in Sweden indicating a weak barrier to gene flow, but two highly genetically and phenotypically divergent, and partly spatially overlapping clusters in Spain suggesting a much stronger barrier to gene flow. The absence of Spanish early-generation hybrids supported strong isolation, but a low level of gene flow is evident from molecular data. In both countries, highly differentiated loci were located in both shared and country-specific chromosomal inversions but were also present in collinear regions. Despite being considered the same species and showing similar levels of phenotypic divergence, the Spanish ecotypes are much closer to full reproductive isolation than the Swedish ones. Barriers to gene flow of very different strengths between ecotypes within the same species might be explained by dissimilarities in the spatial arrangement of habitats, the selection gradients or the ages of the systems.}, author = {Raffini, Francesca and De Jode, Aurélien and Johannesson, Kerstin and Faria, Rui and Zagrodzka, Zuzanna B. and Westram, Anja M and Galindo, Juan and Rolán-Alvarez, Emilio and Butlin, Roger K.}, issn = {1365-294X}, journal = {Molecular Ecology}, number = {21}, publisher = {Wiley}, title = {{Phenotypic divergence and genomic architecture between parallel ecotypes at two different points on the speciation continuum in a marine snail}}, doi = {10.1111/mec.70025}, volume = {34}, year = {2025}, } @misc{20103, abstract = {Official implementation, windowed MSAs, and the predictions as reported in the manuscript titled "Improving Prediction Accuracy in Chimeric Proteins with Windowed Multiple Sequence Alignment". (2025-06-27)}, author = {Vedula, Sanketh and Bronstein, Alexander and Marx, Ailie}, publisher = {Harvard Dataverse}, title = {{Replication Data for: "Improving Prediction Accuracy in Chimeric Proteins with Windowed Multiple Sequence Alignment"}}, doi = {10.7910/DVN/DYEBVM}, year = {2025}, } @misc{20107, abstract = {This repository contains the data and scripts required to reproduce the results of the manuscript "Sustainable Development Key to Limiting Climate Change-Driven Wildfire Damages" submitted to the Environmental Research Climate Journal (ERCL). }, author = {Hwong, Yi-Ling and Byers, Edward and Werning, Michaela and Quilcaille, Yann}, publisher = {Zenodo}, title = {{Data - Sustainable Development Key to Limiting Climate Change-Driven Wildfire Damages}}, doi = {10.5281/ZENODO.13988679}, year = {2025}, } @article{20116, abstract = {Auxin regulates various aspects of plant growth and development by modulating the transcription of target genes through the degradation of auxin/indole-3-acetic acid (Aux/IAA) repressors via the 26S proteasome. Proteasome regulator 1 (PTRE1), a positive regulator of proteasome activity, has been implicated in auxin-mediated proteasome suppression; however, the mechanism by which auxin modulates PTRE1 function remains unclear. Here, we demonstrate that auxin promotes the interaction between germin-like protein 1 (GLP1) and PTRE1, facilitating PTRE1 retention at the plasma membrane. The relocation of PTRE1 results in reduced nuclear 26S proteasome activity, and thus the attenuated Aux/IAA degradation and altered Aux/IAA homeostasis, ultimately resulting in suppressed auxin-mediated transcriptional regulation. Our findings uncover a previously uncharacterized regulatory axis in auxin signaling that controls Aux/IAA protein stability, functioning alongside the TIR1- and TRANSMEMBRANE KINASE 1 (TMK1)-mediated pathways, and highlight the coordination of auxin signaling from the cell surface to the nucleus via auxin-induced PTRE1 relocation, which fine-tunes Aux/IAA protein homeostasis and auxin responses.}, author = {Xu, Faqing and Yu, Yongqiang and Guan, Bin and Xu, Tongda and Xu, Zhihong and Xue, Hongwei}, issn = {2211-1247}, journal = {Cell Reports}, number = {8}, publisher = {Elsevier}, title = {{Germin-like protein 1 interacts with proteasome regulator 1 to regulate auxin signaling by controlling Aux/IAA homeostasis}}, doi = {10.1016/j.celrep.2025.116056}, volume = {44}, year = {2025}, } @phdthesis{20117, author = {Wang, Yiqun}, issn = {2663-337X}, pages = {108}, publisher = {Institute of Science and Technology Austria}, title = {{The role of dynamin related protein 2A in cytokinin regulated plant growth and development}}, doi = {10.15479/AT-ISTA-20117}, year = {2025}, } @article{20143, abstract = {Bacteria and archaea deploy diverse antiviral defense systems, many of which remain mechanistically uncharacterized. Here, we characterize Kiwa, a widespread two-component system composed of the transmembrane sensor KwaA and the DNA-binding effector KwaB. Cryogenic electron microscopy (cryo-EM) analysis reveals that KwaA and KwaB assemble into a large, membrane-associated supercomplex. Upon phage binding, KwaA senses infection at the membrane, leading to KwaB binding of ejected phage DNA and inhibition of replication and late transcription, without inducing host cell death. Although KwaB can bind DNA independently, its antiviral activity requires association with KwaA, suggesting spatial or conformational regulation. We show that the phage-encoded DNA-mimic protein Gam directly binds and inhibits KwaB but that co-expression with the Gam-targeted RecBCD system restores protection by Kiwa. Our findings support a model in which Kiwa coordinates membrane-associated detection of phage infection with downstream DNA binding by its effector, forming a spatially coordinated antiviral mechanism.}, author = {Zhang, Zhiying and Todeschini, Thomas C. and Wu, Yi and Kogay, Roman and Naji, Ameena and Cardenas Rodriguez, Joaquin and Mondi, Rupavidhya and Kaganovich, Daniel and Taylor, David W. and Bravo, Jack Peter Kelly and Teplova, Marianna and Amen, Triana and Koonin, Eugene and Patel, Dinshaw J. and Nobrega, Franklin L.}, issn = {1097-4172}, journal = {Cell}, number = {21}, pages = {5862--5877.e23}, publisher = {Elsevier}, title = {{Kiwa is a membrane-embedded defense supercomplex activated at phage attachment sites}}, doi = {10.1016/j.cell.2025.07.002}, volume = {188}, year = {2025}, }