Biology subjects

Horn, N.

Publications and source records attributed to Horn, N..

5 recordsLinked to original sources

bioRxiv2026

Assessing seabird and shorebird vulnerability to offshore wind farms in Brazil: A decision-support framework for environmental licensing

Environmental concerns and the need to mitigate the effects of climate change have driven the adoption of renewable energy sources, such as offshore wind farms (OWFs), making it essential to assess their overlap with seabird habitats to estimate potential impacts. This study is the first to estimate the vulnerability of coastal and seabirds to OWFs at a national scale by integrating biological trait data from the literature, spatial occurrence records from citizen science platforms, and expert knowledge (elicited from 23 specialists) into established quantitative risk frameworks. Collision risk and susceptibility scores were calculated at the family and subfamily levels, as well as disturbance and displacement indices by species and susceptibility by state. The groups with the highest collision risk and susceptibility were Fregatidae (0.354; 0.486), Sulidae (0.199; 0.419), Sterninae (0.190; 0.384) and Diomedeidae (0.190; 0.416). The extreme risk for Fregatidae is driven by their specific flight characteristics, with impacts concentrated in the highly frequented southeast and northeast regions. Regarding disturbance and displacement, Limnodromus griseus exhibited the highest national score (MMA: 0.098), while Diomedea dabbenena had the highest global score (IUCN: 0.092), highlighting the critical need to integrate both regional and global conservation statuses. Spatially, the state exhibiting the highest overall vulnerability to OWF impacts was Rio Grande do Sul (23.78; 10.69), a critical hotspot characterized by high species richness and oceanographic productivity. These findings establish an indispensable national baseline for Marine Spatial Planning, reinforcing the need for targeted pre-installation assessments, the identification of sentinel species, and spatially differentiated management during environmental licensing processes.

ecology↗

bioRxiv2026

Genomic diversity, antibiotic resistance, and maturation-dependent adhesion of F18 enterotoxigenic Escherichia coli strains in porcine intestinal cells

Enterotoxigenic Escherichia coli (ETEC) strains expressing F4 and F18 fimbriae are major causes of neonatal and post-weaning diarrhea in swine. Although epithelial maturation influences susceptibility in vivo, its impact on ETEC-host interactions remains poorly defined. This study characterizes emerging F18 ETEC isolates using a differentiated porcine intestinal cell model. Three F18 strains (3EC1, 27EC1, 3247EC), a porcine F4 strain, and human ETEC H10407 were analyzed by comparative genomics for virulence factors, toxin genes, and antimicrobial resistance determinants. Adhesion assays were performed using IPEC-1, IPEC-J2, and Caco-2 cells conditioned to Early (6 days post-confluence, DPC), Mid (9 DPC), and Late (16 DPC) maturation states. Transcription of F18-binding receptors (FUT1, FUT2) was quantified by RT-qPCR. IPEC-1 cells exhibited significantly higher FUT1 and FUT2 expression than IPEC-J2, corresponding to approximately two-fold stronger adhesion by most F18 isolates. Strain 3EC1 showed a distinct adhesion peak at 9 DPC, approaching F4 levels, while F4 and H10407 consistently displayed the highest adhesion across all models. Genomic analyses revealed substantial heterogeneity among F18 strains in fimbrial loci, flagellin, lipopolysaccharide biosynthesis, and antimicrobial resistance. Strain 3EC1 uniquely carried stx2e, and non-classical EAST1 variants were detected in 3EC1 and 3247EC. All F18 isolates encoded hlyE and were {beta}-hemolytic; 3247EC harbored 28 antimicrobial resistance genes. The IPEC-1/IPEC-J2 maturation stages recapitulate age-dependent susceptibility to ETEC, likely driven by FUT1/2 expression levels. The combination of strong adhesion, stx2e, and extensive antimicrobial resistance in F18 strains underscores their evolving virulence and supports this model as a refined platform for studying porcine ETEC pathogenesis. ImportanceETEC remains a leading cause of neonatal and post-weaning diarrhea in swine, yet the biological basis for age-dependent susceptibility is not fully understood. This study demonstrates that maturation of porcine intestinal epithelial cells strongly influences F18 ETEC adhesion, driven in part by developmental regulation of the F18-binding receptors FUT1 and FUT2. By integrating comparative genomics with a physiologically relevant in vitro maturation model, we reveal substantial diversity in virulence and resistance among F18 strains, including strong adhesion capacity, stx2e, and extensive antimicrobial resistance in strain 3EC1. These findings highlight the evolution of ETEC toward increased persistence and pathogenic potential in swine populations. The interaction between the maturation-dependent IPEC-1 and IPEC-J2 cell lines and ETEC offers a valuable tool for evaluating intervention strategies to reduce weaning piglet susceptibility to ETEC infection.

microbiology↗

bioRxiv2022

The kinesin motor KIF1C is a putative transporter of the exon junction complex in neuronal cells

Neurons critically depend on regulated RNA localization and tight control of spatio-temporal gene expression to maintain their morphological and functional integrity. Mutations in the kinesin motor protein gene KIF1C cause Hereditary Spastic Paraplegia, an autosomal recessive disease leading to predominant degeneration of the long axons of central motoneurons. In this study we aimed to gain insight into the molecular function of KIF1C and understand how KIF1C dysfunction contributes to motoneuron degeneration. We used affinity proteomics in neuronally differentiated neuroblastoma cells (SH-SY5Y) to identify the protein complex associated with KIF1C in neuronal cells; candidate interactions were then validated by immunoprecipitation and mislocalization of putative KIF1C cargoes was studied by immunostainings. We found KIF1C to interact with all core components of the exon junction complex (EJC); expression of mutant KIF1C in neuronal cells leads to loss of the typical localization distally in neurites. Instead, EJC core components accumulate in the pericentrosomal region, here co-localizing with mutant KIF1C. These findings suggest KIF1C as a neuronal transporter of the EJC. Interestingly, the binding of KIF1C to the EJC is RNA-mediated, as treatment with RNAse prior to immunoprecipitation almost completely abolishes the interaction. Silica-based solid-phase extraction of UV-crosslinked RNA-protein complexes furthermore supports direct interaction of KIF1C with RNA, as recently also demonstrated for kinesin heavy chain. Taken together, our findings are consistent with a model where KIF1C transports mRNA in an EJC-bound and therefore transcriptionally silenced state along neurites, thus providing the missing link between the EJC and mRNA localization in neurons.

neuroscience↗

bioRxiv2021

Synaptotagmin 13 orchestrates pancreatic endocrine cell egression and islet morphogenesis

Epithelial cell egression is important for organ development, but also drives cancer metastasis. Better understandings of pancreatic epithelial morphogenetic programs generating islets of Langerhans aid to diabetes therapy. Here we identify the Ca2+-independent atypical Synaptotagmin 13 (Syt13) as a key driver of endocrine cell egression and islet formation. We detected upregulation of Syt13 in endocrine precursors that correlates with increased expression of unique cytoskeletal components. High-resolution imaging reveals a previously unidentified apical-basal to front-rear repolarization during endocrine cell egression. Strikingly, Syt13 interacts with acetylated tubulin and phosphatidylinositol phospholipids and localizes to the leading-edge of egressing cells. Knockout of Syt13 impairs endocrine cell egression and skews the - to-{beta}-cell ratio. Mechanistically, Syt13 regulates endocytosis to remodel the basement membrane and cell-matrix adhesion at the leading-edge of egressing endocrine cells. Altogether, these findings implicate an unexpected role of Syt13 in regulating cell polarity to orchestrate endocrine cell egression and islet morphogenesis.

developmental biology↗

bioRxiv2017

CiliaCarta: An Integrated And Validated Compendium Of Ciliary Genes

The cilium is an essential organelle at the surface of most mammalian cells whose dysfunction causes a wide range of genetic diseases collectively called ciliopathies. The current rate at which new ciliopathy genes are identified suggests that many ciliary components remain undiscovered. We generated and rigorously analyzed genomic, proteomic, transcriptomic and evolutionary data and systematically integrated these using Bayesian statistics into a predictive score for ciliary function. This resulted in 285 candidate ciliary genes. We found experimental evidence of ciliary associations for 24 out of 36 analyzed candidate proteins. In addition, we show that OSCP1, which has previously been implicated in two distinct non-ciliary functions, causes a cilium dysfunction phenotype when depleted in zebrafish. The candidate list forms the basis of CiliaCarta, a comprehensive ciliary compendium covering 836 genes. The resource can be used to objectively prioritize candidate genes in whole exome or genome sequencing of ciliopathy patients and can be accessed at http://bioinformatics.bio.uu.nl/john/syscilia/ciliacarta/.

bioinformatics↗