@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}, } @techreport{20146, abstract = {This criteria catalogue and the accompanying assessment questions were developed by a working group of KEMÖ (Kooperation E-Medien Österreich, the Austrian Academic Library Consortium). They are intended to support research institutions and organisations in the evaluation of Open Science Infrastructures. The 20 criteria outlined in the catalogue provide a structured basis for making informed decisions regarding the financial support of these infrastructures. The assessment questions are intended to be completed by Open Science Infrastructures and can be shared with them accordingly.}, author = {Gredler, Paul and Kaier, Christian and Danowski, Patrick and Zoyer, Michael and Rieck, Katharina and Ferus, Andreas and Rosenberger, Elisabeth and Löffler, Alexander and Hofer, Lisa and Still, Laura}, publisher = {Zenodo}, title = {{Catalogue of criteria for assessing the funding eligibility of Open Science infrastructures}}, doi = {10.5281/zenodo.15269364}, year = {2025}, } @phdthesis{20149, abstract = {Immune responses depend on the coordinated and efficient migration of leukocytes. These cells, which are embedded and tightly confined within tissues, must navigate and traverse diverse and complex three-dimensional environments. Leukocytes adapt their locomotory behavior to the mechanical, geometrical, and biochemical characteristics of their surroundings. In low-density environments, where the pore size of the interstitial matrix allows free passage, these cells position the nucleus directly behind the lamellipodium, the protrusive actin structure that forms the leading front of the cell. In this configuration, they use the nucleus as a gauge to identify the path of least resistance. Here, we show that in high-density environments, where the pore size precludes free passage of the cell body, leukocytes reposition the microtubule-organizing center (MTOC) and associated organelles in front of the nucleus. In this configuration, they use actin structures protruding orthogonally to the direction of migration in order to open a path for the cell body. We identify two distinct actin populations that serve this purpose at different subcellular localizations. At the leading edge, local indentation of the plasma membrane leads to recruitment of the Wiskott-Aldrich syndrome protein (WASp), which, via Arp2/3, results in the formation of individual actin foci. At the cell body, actin polymerization is triggered by DOCK8, a Cdc42 exchange factor, resulting in the formation of a central actin pool. We demonstrate that the central and peripheral actin pools are functionally communicating and that depletion of the central actin pool leads to increased actin accumulation at the cell front, resulting in excessive extension of the leading edge.}, author = {Dos Reis Rodrigues, Patricia}, issn = {2663-337X}, pages = {114}, publisher = {Institute of Science and Technology Austria}, title = {{Coordination of protrusive forces in immune cell migration }}, doi = {10.15479/AT-ISTA-20149}, year = {2025}, } @article{20154, abstract = {In long-lived mammals, including humans, brain cell homeostasis is critical for maintaining brain function throughout life. Most neurons are generated during development and must maintain their cellular identity and plasticity to preserve brain function. Although extensive studies indicate the importance of recycling and regenerating cellular molecules to maintain cellular homeostasis, recent evidence has shown that some proteins and RNAs do not turn over for months and even years. We propose that these long-lived cellular molecules may be the basis for maintaining brain function in the long term, but also a potential convergent target of brain aging. We highlight key discoveries and challenges, and propose potential directions to unravel the mystery of brain cell longevity.}, author = {Hetzer, Martin W and Toda, Tomohisa}, issn = {1878-108X}, journal = {Trends in Neurosciences}, number = {9}, pages = {645--654}, publisher = {Elsevier}, title = {{Long-lived cellular molecules in the brain}}, doi = {10.1016/j.tins.2025.07.004}, volume = {48}, year = {2025}, } @article{20155, abstract = {We study time averages for the norm of solutions to kinetic Fokker–Planck equations associated with general Hamiltonians. We provide fully explicit and constructive decay estimates for systems subject to a confining potential, allowing fat-tail, subexponential and (super-)exponential local equilibria, which also include the classic Maxwellian case. The key step in our estimates is a modified Poincaré inequality, obtained via a Lions–Poincaré inequality and an averaging lemma.}, author = {Brigati, Giovanni and Stoltz, Gabriel}, issn = {1095-7154}, journal = {SIAM Journal on Mathematical Analysis}, number = {4}, pages = {3587--3622}, publisher = {Society for Industrial and Applied Mathematics}, title = {{How to construct explicit decay rates for kinetic Fokker–Planck equations?}}, doi = {10.1137/24M1700351}, volume = {57}, year = {2025}, } @phdthesis{20167, author = {Schön, Hanna}, isbn = {978-3-99078-061-9}, issn = {2663-337X}, pages = {171}, publisher = {Institute of Science and Technology Austria}, title = {{The ER complex SUTU-7/MACO-1 regulates the fate of mRNAs encoding GPCRs}}, doi = {10.15479/AT-ISTA-20167}, year = {2025}, } @article{20182, abstract = {Sex chromosomes have evolved many times throughout the tree of life, and understanding what has shaped their unusual morphological, sequence, and regulatory features has been a long-standing goal. Most early insights into insect sex chromosome biology came from a few model species, such as the fruit fly Drosophila melanogaster, which limited broad-scale evolutionary inferences. More recently, extensive comparative genomics studies have uncovered several unexpected patterns, which we highlight in this review. First, we describe the conservation of the ancestral X chromosome over 450 million years but also its recurrent turnover (i.e. its reversal to an autosome when a new X chromosome arose) in at least one order. We then summarize classical and more recent findings on how insects modulate the expression of X-linked genes following the degradation of the Y chromosome and how the diverse mechanisms of dosage compensation identified may elucidate important principles of sex chromosome regulatory evolution.}, author = {Toups, Melissa A and Vicoso, Beatriz}, issn = {2214-5753}, journal = {Current Opinion in Insect Science}, publisher = {Elsevier}, title = {{Insect sex chromosome evolution: Conservation, turnover, and mechanisms of dosage compensation}}, doi = {10.1016/j.cois.2025.101411}, volume = {72}, year = {2025}, } @article{20183, abstract = {The unequal segregation of organelles has been proposed to be an intrinsic mechanism that contributes to cell fate divergence during asymmetric cell division; however, in vivo evidence is sparse. Using super-resolution microscopy, we analysed the segregation of organelles during the division of the neuroblast QL.p in C. elegans larvae. QL.p divides to generate a daughter that survives, QL.pa, and a daughter that dies, QL.pp. We found that mitochondria segregate unequally by density and morphology and that this is dependent on mitochondrial dynamics. Furthermore, we found that mitochondrial density in QL.pp correlates with the time it takes QL.pp to die. We propose that low mitochondrial density in QL.pp promotes the cell death fate and ensures that QL.pp dies in a highly reproducible and timely manner. Our results provide in vivo evidence that the unequal segregation of mitochondria can contribute to cell fate divergence during asymmetric cell division in a developing animal.}, author = {Segos, Ioannis and Van Eeckhoven, Jens and Berger, Simon and Mishra, Nikhil and Lambie, Eric J. and Conradt, Barbara}, issn = {2041-1723}, journal = {Nature Communications}, publisher = {Springer Nature}, title = {{Unequal segregation of mitochondria during asymmetric cell division contributes to cell fate divergence in sister cells in vivo}}, doi = {10.1038/s41467-025-62484-5}, volume = {16}, year = {2025}, } @article{20184, abstract = {Specialized DNA polymerases facilitate various cellular processes. Despite extensive research, the mutagenic effects of these error-prone enzymes on genomes are not fully understood. Here we show that Pol IV promotes genomic instability in Pseudomonas aeruginosa by misincorporating oxidized guanine nucleotides. This activity led to a distinctive mutational signature, characterized by A-to-C transversions occurring preferentially at AT sites flanked by a 5’G and/or 3’C. Furthermore, Pol IV preferentially targeted pathogenicity genes located at specific chromosomal locations near the replication termination region and rRNA-encoding operons. Half of the mutation events catalyzed by Pol IV impaired gene function. This can be attributed to the bias of Pol IV for mutating codons with its preferred sequence contexts, leading to substitutions to unreactive alanine and glycine residues. Remarkably, mutation signatures identified for Pol IV were found in clinical isolate genomes of P. aeruginosa, providing compelling evidence for its role in genetic diversification during pathogen adaptation.}, author = {Castell, Sofía D. and Fernandez, Consuelo M. and Tumas, Ignacio N. and Margara, Lucía M. and Miserendino, Maria C and Ceschin, Danilo G. and Pezza, Roberto J. and Monti, Mariela R.}, issn = {2399-3642}, journal = {Communications Biology}, publisher = {Springer Nature}, title = {{The low-fidelity DNA Pol IV accelerates evolution of pathogenicity genes in Pseudomonas aeruginosa}}, doi = {10.1038/s42003-025-08589-5}, volume = {8}, year = {2025}, } @article{20185, abstract = {We show a local rigidity result for the integrability of symplectic billiards. We prove that any domain which is close to an ellipse, and for which the symplectic billiard map is rationally integrable must be an ellipse as well. This is in spirit of the result of [2] for Birkhoff billiards.}, author = {Tsodikovich, Daniel}, issn = {1050-6926}, journal = {Journal of Geometric Analysis}, number = {10}, publisher = {Springer Nature}, title = {{Local rigidity for symplectic billiards}}, doi = {10.1007/s12220-025-02148-4}, volume = {35}, year = {2025}, } @article{20186, abstract = {Enforcement of information-flow policies has been extensively studied by language-based approaches over the past few decades. In this paper, we propose an alternative, novel, general, and effective approach using enforcement of hyperproperties– a powerful formalism for expressing and reasoning about a wide range of information-flow security policies. We study black- vs. gray- vs. white-box enforcement of hyperproperties expressed by nondeterministic finite-word hyperautomata (NFH), where the enforcer has null, some, or complete information about the implementation of the system under scrutiny. Given an NFH, in order to generate a runtime enforcer, we reduce the problem to controller synthesis for hyperproperties and subsequently to the satisfiability problem for quantified Boolean formulas (QBFs). The resulting enforcers are transferable with low-overhead. We conduct a rich set of case studies, including information-flow control for JavaScript code, as well as synthesizing obfuscators for control plants.}, author = {Hsu, Tzu Han and Oliveira Da Costa, Ana A and Wintenberg, Andrew and Bartocci, Ezio and Bonakdarpour, Borzoo}, issn = {1432-0525}, journal = {Acta Informatica}, number = {3}, publisher = {Springer Nature}, title = {{Gray-box runtime enforcement of hyperproperties}}, doi = {10.1007/s00236-025-00502-1}, volume = {62}, year = {2025}, } @article{20187, abstract = {Very long-chain fatty acids (VLCFAs), being constituents of different types of lipids, are critical factors in plant development, presumably due to their impact on the endomembrane system. The VLCFAs are synthesized in the endoplasmic reticulum by a heterotetrameric enzymatic complex including β-ketoacyl CoA reductase 1 (KCR1), whose mutant is lethal. Here, we describe the ectopic shoot meristems (esm) mutant, a viable kcr1 allele presumably affecting surface properties of the KCR1 protein. This kcr1-2 mutant shows reduced fatty acyl elongation that impacts VLCFAs. The kcr1-2 plants show severe defects during different stages of development, which all correlate with defects in polar localization and subcellular trafficking of PIN auxin transporters and resulting asymmetric auxin distribution. Detailed analysis of KCR1 expression and patterning defects in kcr1-2 suggests that KCR1 plays a role in delineating boundaries around meristematic and specialized differentiating tissues, including root and shoot meristems, initiating lateral roots, lateral root primordia, and trichomes. In these contexts, KCR1-produced VLCFAs may act in a non-cell-autonomous manner. Viable kcr1-2 represents a useful tool to study VLCFA roles in plant development and highlights VLCFAs as critical developmental factors at the interface of cell polarity and tissue development.}, author = {Babic, David and Abualia, Rashed and Fiedler, Lukas and Qi, Linlin and Tellier, Frédérique and Smoljan, Adrijana and Rakusova, Hana and Valošek, Petr and Han, Huibin and Benková, Eva and Faure, Jean Denis and Friml, Jiří}, issn = {1365-313X}, journal = {Plant Journal}, number = {3}, publisher = {Wiley}, title = {{Biosynthesis of very long-chain fatty acids is required for Arabidopsis auxin-mediated embryonic and post-embryonic development}}, doi = {10.1111/tpj.70396}, volume = {123}, year = {2025}, } @article{20188, abstract = {Collective cell migration is coordinated by the front-to-rear intercellular propagation of EGFR-Ras-ERK pathway activation. However, the molecular mechanisms integrating front-to-rear information into this intercellular signaling cascade, particularly the determinants of cellular front-side specification, remain elusive. We visualized the activity of EGFR, Ras, Rac1 and Rab5A (hereafter Rab5) by using FRET biosensors and chemogenetic tools. Whereas EGFR activation was uniformly observed within cells, Ras activation was biased to the front side within cells. The polarized Ras activation depended on Merlin and Rac1, which also showed front-biased activation. Furthermore, Rab5, a crucial regulator of cell migration, demonstrated similar front-biased activation and was found to function downstream of Ras while being necessary for Rac1 activation. Thus, the positive feedback loop consisting of Ras, Rab5 and Rac1 is activated primarily at the front of collectively migrating cells. These findings offer new spatio-temporal insight into processing front–rear information during collective cell migration.}, author = {Jikko, Yuya and Deguchi, Eriko and Matsuda, Kimiya and Hino, Naoya and Tsukiji, Shinya and Matsuda, Michiyuki and Terai, Kenta}, issn = {1477-9137}, journal = {Journal of Cell Science}, number = {15}, publisher = {The Company of Biologists}, title = {{Front-biased activation of the Ras-Rab5-Rac1 loop coordinates collective cell migration}}, doi = {10.1242/jcs.263779}, volume = {138}, year = {2025}, } @inproceedings{20189, abstract = {Certification was made mandatory for the first time in the latest hardware model checking competition. In this case study, we investigate the trade-offs of requiring certificates for both passing and failing properties in the competition. Our evaluation shows that participating model checkers were able to produce compact, correct certificates that could be verified with minimal overhead. Furthermore, the certifying winner of the competition outperforms the previous non-certifying state-of-the-art model checker, demonstrating that certification can be adopted without compromising model checking efficiency.}, author = {Froleyks, Nils and Yu, Zhengqi and Preiner, Mathias and Biere, Armin and Heljanko, Keijo}, booktitle = {37th International Conference on Computer Aided Verification}, isbn = {9783031986673}, issn = {1611-3349}, location = {Zagreb, Croatia}, pages = {281--295}, publisher = {Springer Nature}, title = {{Introducing certificates to the hardware model checking competition}}, doi = {10.1007/978-3-031-98668-0_14}, volume = {15931}, year = {2025}, } @article{20192, abstract = {We study the physical origin and spectroscopic impact of extreme nebular emission in high-redshift galaxies. The nebular continuum, which can appear during an extreme starburst, is of particular importance as it tends to redden UV slopes and has a significant contribution to the UV luminosities of galaxies. Furthermore, its shape can be used to infer the gas density and temperature of the interstellar medium. First, we provide a theoretical background, showing how different stellar populations (SPS models, initial mass functions (IMFs), and stellar temperatures) and nebular conditions impact observed galaxy spectra. We demonstrate that, for systems with strong nebular continuum emission, 1) UV fluxes can increase by up to 0.7~mag (or more in the case of hot/massive stars) above the stellar continuum, which may help reconcile the surprising abundance of bright high-redshift galaxies and the elevated UV luminosity density at z>10, 2) at high gas densities, UV slopes can redden from \beta<-2.5 to \beta\sim-1, 3) observational measurements of \xi_{\rm ion} are gross underestimates, and 4) UV downturns from two-photon emission can masquerade as damped Ly\alpha systems. Second, we present a dataset of 58 galaxies observed with NIRSpec on JWST at 2.510 galaxies, finding that UV slopes and UV downturns are in some cases redder or steeper than expected from SPS models, which may hint at more exotic (e.g. hotter/more massive stars or AGN) ionizing sources.}, author = {Katz, Harley and Cameron, Alex J. and Saxena, Aayush and Barrufet, Laia and Choustikov, Nicholas and Cleri, Nikko J. and De Graaff, Anna and Ellis, Richard S. and Fosbury, Robert A.E. and Heintz, Kasper E. and Maseda, Michael and Matthee, Jorryt J and Mcconachie, Ian and Oesch, Pascal A.}, issn = {2565-6120}, journal = {The Open Journal of Astrophysics}, publisher = {Maynooth Academic Publishing}, title = {{21 Balmer Jump Street: The nebular continuum at high redshift and implications for the bright galaxy problem, UV continuum slopes, and early stellar populations}}, doi = {10.33232/001c.142570}, volume = {8}, year = {2025}, } @article{20193, abstract = {Understanding the rapid formation of supermassive black holes in the early Universe requires insights into stellar mass growth in host galaxies. Here we present NIRSpec rest-frame optical spectra and NIRCam imaging from JWST of two galaxies at z > 6, both hosting moderate-luminosity quasars. These galaxies exhibit Balmer absorption lines, like low-redshift post-starburst galaxies. Our analyses of the medium-resolution spectra and multiband photometry show that the bulk of the stellar mass (log(M*/M☉) ≥ 10.6) formed in starburst episodes at redshift 9 and 7. One of the galaxies shows a clear Balmer break and lacks spatially resolved Hα emission. It falls well below the star-formation main sequence at z = 6, indicating quiescence. The other is transitioning to quiescence; together, these massive galaxies are among the most distant post-starburst systems known. The blueshifted wings of the quasar [O iii] emission lines indicate quasar-driven outflow, which possibly influences star formation. Direct stellar velocity dispersion measurements reveal that one galaxy follows the local black hole mass versus σ* relation whereas the other is overmassive. The existence of massive post-starburst galaxies hosting billion-solar-mass black holes in short-lived quasar phases indicates that supermassive black holes and host galaxies played a principal role in each other’s rapid early formation.}, author = {Onoue, Masafusa and Ding, Xuheng and Silverman, John D. and Matsuoka, Yoshiki and Izumi, Takuma and Strauss, Michael A. and Ward, Charlotte and Phillips, Camryn L. and Ito, Kei and Andika, Irham T. and Aoki, Kentaro and Arita, Junya and Baba, Shunsuke and Bieri, Rebekka and Bosman, Sarah E.I. and Eilers, Anna Christina and Fujimoto, Seiji and Habouzit, Melanie and Haiman, Zoltán and Imanishi, Masatoshi and Inayoshi, Kohei and Iwasawa, Kazushi and Jahnke, Knud and Kashikawa, Nobunari and Kawaguchi, Toshihiro and Kohno, Kotaro and Lee, Chien Hsiu and Li, Junyao and Lupi, Alessandro and Lyu, Jianwei and Nagao, Tohru and Overzier, Roderik and Schindler, Jan Torge and Schramm, Malte and Scoggins, Matthew T. and Shimasaku, Kazuhiro and Toba, Yoshiki and Trakhtenbrot, Benny and Trebitsch, Maxime and Treu, Tommaso and Umehata, Hideki and Venemans, Bram and Vestergaard, Marianne and Volonteri, Marta and Walter, Fabian and Wang, Feige and Yang, Jinyi and Zhang, Haowen}, issn = {2397-3366}, journal = {Nature Astronomy}, pages = {1541--1552}, publisher = {Springer Nature}, title = {{A post-starburst pathway for the formation of massive galaxies and black holes at z > 6}}, doi = {10.1038/s41550-025-02628-1}, volume = {9}, year = {2025}, }