@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}, } @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}, }