Search bioRxiv⌕ Search

Biology subjects

Wilkinson, C.

Publications and source records attributed to Wilkinson, C..

5 recordsLinked to original sources

MacroMove: a global database of animal movement across taxa and movement types

Animal movement is a key ecological process that shapes species distributions and interactions and connects resources, populations and habitats, underpinning ecosystem functioning and stability. While foraging, dispersal, and migration are the most widely studied movement types, they operate at distinct spatial and temporal scales, and no single resource currently integrates these processes across taxa, traits, and ecosystems. We present MacroMove, a comprehensive global movement database containing 92,207 observations from 4,329 (4,167 using GBIF backbone) species, spanning 36 classes and 648 families across 205 countries, with data sourced from 6,234 references and 36 meta-analyses/databases. It includes both vertebrates and invertebrates from terrestrial, freshwater, and marine environments. The database includes various movement metrics - home range area, dispersal distance, migration distance, day range, routine speed and maximum speed - including summary statistics (e.g. mean, median, maximum) where available. Records are reported at individual, population, or species levels and include standardised metadata describing species identity (binomial name, class, family), research methods (e.g. sampling method, sampling level and sampling dates) and location (e.g. country, location and coordinates). The dataset was assembled from published meta-analyses/databases and original studies included in these meta-analyses. Trait information (body mass and locomotion mode) from original studies and associated metadata was incorporated, with additional data sourced from established trait databases and reputable online resources. In the final dataset, body mass is available for 98 % and locomotion for 100% of species. Taxonomy was harmonised using the Global Biodiversity Information Facility (GBIF) backbone taxonomy. The database is supplied in comma-delimited text (.csv) format to maximise accessibility and compatibility with a wide range of workflows. By consolidating existing movement data into a single, standardised and openly accessible resource, MacroMove fills a major gap in available biodiversity data. It serves as a practical and extensible foundation for synthesising movement information across taxa and ecosystems, advancing data-driven research on the ecological and evolutionary correlates of animal movement.

ecology↗

A catastrophic marine mortality event caused by a complex algal bloom including the novel brevetoxin producer, Karenia cristata (Dinophyceae)

Harmful algal blooms of Karenia brevis (Dinophyceae) are a global anomaly, occurring in one location worldwide, causing severe marine and acute human impacts via brevetoxins (BTX). During 2025 an unprecedented, currently ongoing, mass marine mortality occurred in South Australia, across an area of [~]20,000 km2, persisting for >6 months, resulting in the deaths of [~]106 marine animals of >550 taxa, with human health impacts. Using custom metabarcoding, long-read sequencing and targeted quantitative PCR, we characterized the microalgal assemblage. Karenia cristata dominated over the sampling area, in an assemblage with four other Karenia species with varied abundances spatially and temporally. High abundances of K. cristata appeared in the austral autumn, and hydrodynamic processes appear to have entrained cells coastward in the semi-enclosed seas. We isolated the species and characterized it using light and electron microscopy, liquid chromatography mass spectrometry and toxicity assays. We show for the first time that the rare and little known K. cristata produces significant BTX with a profile (BTX-2, -3, -B5), differing from K. brevis, with toxicological effects. These findings reveal a novel, significant BTX-producing Karenia, which considering its substantial detrimental marine ecosystem impacts, is an emerging international threat with unknown consequences in changing ocean conditions.

ecology↗

Paracrine role for endothelial IGF-1 receptor in white adipocyte beiging

There are at least two distinct types of thermogenic adipocyte in mammals: a pre-existing form established during development, termed classical brown adipocytes and an inducible form, beige adipocytes1-3. Various environmental cues can stimulate a process frequently referred to as beiging of white adipose tissue (WAT), leading to enhanced thermogenesis and obesity resistance 4, 5. Whilst beiging of WAT as a therapeutic goal for obesity and obesity-related complications has attracted much attention6-9; therapeutics stimulating beiging without deleterious side-effects remain elusive10. The endothelium lines all blood vessels and is therefore in close proximity to all cells. Many studies support the possibility that the endothelium acts as a paracrine organ11-14. We explored the potential role of endothelial insulin-like growth factor-1 receptor (IGF-1R) as a paracrine modulator of WAT phenotype. Here we show that a reduction in endothelial IGF-1R expression in the presence of nutrient excess leads to white adipocyte beiging, increases whole-body energy expenditure and enhances insulin sensitivity via a non-cell autonomous paracrine mechanism. We demonstrate that this is mediated by endothelial release of malonic acid, which we show, using prodrug analogues, has potentially therapeutically-relevant properties in the treatment of metabolic disease.

cell biology↗

Loss of ELK1 has differential effects on age-dependent organ fibrosis and integrin expression

ETS domain-containing protein-1 (ELK1) is a transcriptional repressor important in regulating v{beta}6 integrin expression. v{beta}6 integrins activate the profibrotic cytokine Transforming Growth Factor {beta}1 (TGF{beta}1) and are increased in the alveolar epithelium in Idiopathic Pulmonary Fibrosis (IPF). IPF is a disease associated with ageing and therefore we hypothesised that aged animals lacking Elk1 globally would develop spontaneous fibrosis in organs where v{beta}6-mediated TGF{beta} activation has been implicated.\n\nHere we identify that Elk1-knockout (Elk1-/0) mice aged to one year developed spontaneous fibrosis in the absence of injury in both the lung and the liver but not in the heart or kidneys. The lungs of Elk1-/0 aged mice demonstrated increased collagen deposition, in particular collagen 31, located in small fibrotic foci and thickened alveolar walls. Despite the liver having relatively low global levels of ELK1 expression, Elk1-/0 animals developed hepatosteatosis and fibrosis. The loss of Elk1 also had differential effects on Itgb1, Itgb5 and Itgb6 genes expression in the four organs potentially explaining the phenotypic differences in these organs. To understand the potential causes of reduced ELK1 in human disease we exposed human cells and murine lung slices to cigarette smoke extract which lead to reduced ELK1 expression which may explain the loss of ELK1 in human disease.\n\nThese data support a fundamental role for ELK1 in protecting against the development of progressive fibrosis via transcriptional regulation of beta integrin subunit genes, and demonstrate that loss of ELK1 can be caused by cigarette smoke.

pathology↗

Trypanosoma brucei Pex13.2 is an accessory peroxin that functions in the import of PTS2 proteins and localizes to subdomains of the glycosome

Kinetoplastid parasites including Trypanosoma brucei, Trypanosoma cruzi and Leishmania harbor unique organelles known as glycosomes, which are evolutionarily related to peroxisomes. Glycosome/peroxisome biogenesis is mediated by proteins called peroxins that facilitate organelle formation, proliferation and degradation, and import of proteins housed therein. Import of matrix proteins occurs via one of two pathways that are dictated by their peroxisome targeting sequence (PTS). In PTS1 import, a C-terminal tripeptide sequence, most commonly SKL, is recognized by the soluble receptor Pex5. In PTS2 import, a less conserved N-terminal sequence is recognized by Pex7. The soluble receptors deliver their cargo to the import channel consisting minimally of Pex13 and Pex14. While much of the import process is conserved, kinetoplastids are the only organisms to have two Pex13s, TbPex13.1 and TbPex13.2. In previous studies, GFP-tagged TbPex13.1 localized to glycosomes and silencing either protein in the stage of the parasite that lives in the mammalian bloodstream impaired glycosome protein import and slowed parasite growth. While these findings suggest Pex13s are involved in protein import, the mechanisms by which they function are unknown and it is unclear why kinetoplastids would require two Pex13s. In this work, we demonstrate that TbPex13.2 is associated with the glycosome membrane with its N-terminus facing the cytoplasm. Super-resolution microscopy reveals that TbPex13.2 localizes to a few (1-3) foci per glycosome and import of PTS2 proteins was disrupted in TbPex13.2-deficient cells suggesting it may be an accessory factor for PTS2 import.

cell biology↗