Biology subjects

Casey, J. M.

Publications and source records attributed to Casey, J. M..

7 recordsLinked to original sources

bioRxiv2026

ASYNCHRONOUS TROPHIC NICHE SHIFTS AMONG INVERTEBRATE-FEEDING FISHES ACROSS A CORAL COVER GRADIENT

Unraveling the links between habitat structure, resource availability and the trophic niche is key to anticipate the effects of global change on ecosystems. On coral reefs, recurrent coral bleaching and increasing anthropogenic pressures have led to rapid losses of structural complexity, with implications for food web dynamics. Invertebrate-feeding fishes are one of the most diverse guilds, and benthic invertebrate communities may be reshuffled by coral loss. Ecological theory suggests that, within the same guild, species respond to habitat and resource change in synchrony, resulting in less partitioning and more functional redundancy at the community level. However, whether the trophic niches of invertivorous reef fishes shift across a gradient of reef condition remains undocumented. Here, we combine otolithometry, gut content metabarcoding, and stable isotope analysis to investigate the performance and trophic plasticity and synchrony of six invertivorous fishes from French Polynesia across various states of coral cover. Most species exhibited distinct niche breath in high versus low cover sites. However, the direction and magnitude of trophic niche differences between high and low coral cover sites varied among species, indicating asynchronous differences in trophic niche breadth across the guild. Our findings reveal that habitat loss may not result in one universal response, even within the same guild. Rather, reef invertivores may have asynchronous trophic differentiation, allowing the maintenance of interspecific coexistence even on degraded reefs. Together, these findings suggest that asynchronous trophic responses may contribute to the resilience of coral reef food webs and help sustain biodiversity under habitat degradation.

ecology↗

bioRxiv2026

Energy quality shapes biodiversity across coastal oceans

Earth's biodiversity is distributed unevenly, typically peaking in warm, vegetated, and stable environments. This has frequently been linked to energy availability, which boosts productivity, bolsters populations, and facilitates coexistence. Here, we examine the relationship between energy and biodiversity across coastal oceans using particulate organic matter biogeochemistry and environmental DNA. We reveal that energy quantity (concentrations of carbon, nitrogen, and hydrolyzable amino acids) and salinity, two variables that co-vary with freshwater inflow, jointly predict species richness at regional and global scales. Biodiversity was lowest at sites and locations with high energy inflow and low salinity, suggesting that environmental filtering associated with the osmotic stress induced by freshwater inflow outweighs raw resource availability in governing species richness. Independent of this gradient, however, energy quality (defined via C:N ratios, {delta}C values, and amino acid profiles) was associated with higher biodiversity. Labile, protein-rich, marine-derived resources supported higher biodiversity across all taxa at the regional scale, and a larger number of planktonic consumer taxa at both regional and global scales. High energy quality sites were also enriched in key planktonic groups such as calanoid and cyclopoid copepods, suggesting that these sites act as hotspots of planktonic biodiversity across coastal seascapes. Our findings suggest that few species can directly harness the plentiful resources provided by terrestrial subsidies in coastal oceans because they arrive in low salinity waters. In turn, high-quality food attracts a diverse range of consumers, which may seed the patchy foraging hotspots that characterize open-water food webs. Altered coastal hydrodynamics and biogeochemistry may therefore affect nearshore biodiversity, food webs, and fisheries.

ecology↗

bioRxiv2026

Ubiquitous trophic niche partitioning drives species coexistence and biomass on coral reefs

Coral reefs support an extraordinary diversity and biomass of fishes. However, whether species coexist through fine-scale niche partitioning, and whether this impacts ecosystem functioning, remain unresolved. We combined DNA metabarcoding and stable isotope analysis to reconstruct a high-resolution food web and quantify the trophic niches of 2,060 reef fishes across 261 species. We observed extreme trophic partitioning: species pairs diverged by a median of 93% (DNA metabarcoding) and 86% (stable isotopes), consistently overlapping far less than expected by chance. Further, communities with greater trophic complementarity supported higher standing-stock biomass, particularly at high species richness. Our results confirm limiting similarity and trophic complementarity as the driving forces of coexistence and ecosystem functioning in the ocean's most diverse ecological community.

ecology↗

bioRxiv2026

Coral reef ecosystem functions in a human-dominated world

The metabolic processes sustaining coral reefs, from carbonate and primary production to secondary production, remain poorly integrated and rarely quantified simultaneously at global scales. This hampers our ability to predict global responses to accelerating human pressures and manage coral reef functioning. Using metabolic scaling and bioenergetic models applied to surveys from 1,100 reefs worldwide, we provide a global, standardized quantification of 14 ecosystem functions spanning benthic (corals and algae) and fish communities. Our analysis reveals a continuous functional spectrum of global coral reefs organized along four dominant axes: 1) primary production, 2) calcification and habitat structure, 3) secondary biomass production and consumption, and 4) biomass turnover. Functions mediated by fish and benthic communities show weak associations at the global scale rather than tight coupling. Climate stressors reduced calcification and local human impacts lowered secondary production. Yet these directional effects unfolded against a backdrop of substantial natural variability in reef functional configurations, such that heavily and minimally impacted reefs overlap substantially in the global functional space. Temporal analyses across three representative reef systems further revealed that functional trajectories following disturbance are context-dependent, with no universal pattern of recovery across locations. This continuous and context-dependent functional spectrum challenges the notion of universal functional benchmarks and supports locally tailored conservation strategies.

ecology↗

bioRxiv2024

Mutations in PSEN1 predispose inflammation in an astrocyte model of familial Alzheimer's disease through disrupted regulated intramembrane proteolysis

Mutations in PSEN1 cause familial Alzheimers disease with almost complete penetrance. Age at onset is highly variable between different PSEN1 mutations and even within families with the same mutation. Current research into late onset Alzheimers disease implicates inflammation in both disease onset and progression. PSEN1 is the catalytic subunit of {gamma}-secretase, responsible for regulated intramembrane proteolysis of numerous substrates that include cytokine receptors. For this reason, we tested the hypothesis that mutations in PSEN1 impact inflammatory responses in astrocytes, thereby contributing to disease progression. Here, using iPSC-astrocytes, we show that PSEN1 is upregulated in response to inflammatory stimuli, and this upregulation is disrupted by pathological PSEN1 mutations. Using transcriptomic analyses, we demonstrate that PSEN1 mutant astrocytes have an augmented inflammatory profile in their basal state, concomitant with an upregulation of genes coding for regulated intramembrane proteolytic and robust activation of JAK-STAT signalling. Using JAK-STAT2 as an example signalling pathway, we show altered phosphorylation cascades in PSEN1 mutant astrocytes, reinforcing the notion of altered cytokine signalling cascades. Finally, we use small molecule modulators of {gamma}-secretase to confirm a role for PSEN1/{gamma}-secretase in regulating the astrocytic response to inflammatory stimuli. Together, these data suggest that mutations in PSEN1 enhance cytokine signalling via impaired regulated intramembrane proteolysis, thereby predisposing astrocytic inflammatory profiles. These findings support a two-hit contribution of PSEN1 mutations to fAD pathogenesis, not only impacting APP and A{beta} processing but also altering the cellular response to inflammation.

neuroscience↗

bioRxiv2023

Microglia produce the amyloidogenic ABri peptide in familial British dementia

Mutations in ITM2B cause familial British, Danish, Chinese and Korean dementias. In familial British dementia (FBD) a mutation in the stop codon of the ITM2B gene (also known as BRI2) causes a C-terminal cleavage fragment of the ITM2B/BRI2 protein to be extended by 11 amino acids. This fragment, termed amyloid-Bri (ABri), is highly insoluble and forms extracellular plaques in the brain. ABri plaques are accompanied by tau pathology, neuronal cell death and progressive dementia, with striking parallels to the aetiology and pathogenesis of Alzheimers disease. The molecular mechanisms underpinning FBD are ill-defined. Using patient-derived induced pluripotent stem cells, we show that expression of ITM2B/BRI2 is 34-fold higher in microglia than neurons, and 15-fold higher in microglia compared with astrocytes. This cell-specific enrichment is supported by expression data from both mouse and human brain tissue. ITM2B/BRI2 protein levels are higher in iPSC-microglia compared with neurons and astrocytes. Consequently, the ABri peptide was detected in patient iPSC-derived microglial lysates and conditioned media but was undetectable in patient-derived neurons and control microglia. Pathological examination of post-mortem tissue support ABri expression in microglia that are in proximity to pre-amyloid deposits. Finally, gene co-expression analysis supports a role for ITM2B/BRI2 in disease-associated microglial responses. These data demonstrate that microglia are the major contributors to the production of amyloid forming peptides in FBD, potentially acting as instigators of neurodegeneration. Additionally, these data also suggest ITM2B/BRI2 may be part of a microglial response to disease, motivating further investigations of its role in microglial activation. This has implications for our understanding of the role of microglia and the innate immune response in the pathogenesis of FBD and other neurodegenerative dementias including Alzheimers disease.

neuroscience↗

bioRxiv2020

Global gut content data synthesis and phylogeny delineate reef fish trophic guilds

The diversity of life on our planet has produced a remarkable variety of biological traits that characterize different species. Such traits are widely employed instead of taxonomy to increase our understanding of biodiversity and ecosystem functioning. However, for species trophic niches, one of the most critical aspects of organismal ecology, a paucity of empirical information has led to inconsistent definitions of trophic guilds based on expert opinion. Using coral reef fishes as a model, we show that experts often disagree on the assignment of trophic guilds for the same species. Even when broad categories are assigned, 60% of the evaluated trait schemes disagree on the attribution of trophic categories for at least 20% of the species. This disagreement greatly hampers comparability across studies. Here, we introduce a quantitative, unbiased, and fully reproducible framework to define species trophic guilds based on empirical data. First, we synthesize data from community-wide visual gut content analysis of tropical coral reef fishes, resulting in trophic information from 13,961 individuals belonging to 615 reef fish species across all ocean basins. We then use network analysis to cluster the resulting global bipartite food web into distinct trophic guilds, resulting in eight trophic guilds, and employ a Bayesian phylogenetic model to predict trophic guilds based on phylogeny and maximum body size. Our model achieved a misclassification error of 5%, indicating that our approach results in a quantitative and reproducible trophic categorization scheme, which can be updated as new information becomes available. Although our case study is for reef fishes, the most diverse vertebrate consumer group, our approach can be applied to other organismal groups to advance reproducibility in trait-based ecology. As such, our work provides an empirical and conceptual advancement for trait-based ecology and a viable approach to monitor ecosystem functioning in our changing world.

ecology↗