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Robertson, B.

Publications and source records attributed to Robertson, B..

16 recordsLinked to original sources

Social behaviour is a key determinant of virome diversity in New Zealand passerines

Wild birds are important reservoirs of viral diversity and can play key roles in the emergence and dispersal of infectious diseases. Their ability to harbour multiple infections without overt disease, combined with their mobility and ecological interactions, creates opportunities for viruses to spread across species and geographic regions. Despite this, the factors shaping avian viromes remain poorly understood, particularly in Aotearoa New Zealand, where endemic and introduced bird species coexist within a relatively isolated ecosystem. This study used metatranscriptomic sequencing to characterise the viromes of 443 endemic and introduced passerines sampled over four years within a shared ecological setting. A total of 217 viruses, representing 69 viral species across 14 families, were identified, including 54 previously undescribed viruses. Many were closely related to viruses reported from birds in Asia, North America, Europe and Australia, suggesting historical or ongoing viral exchange through migration, co-divergence or cross-species transmission. Introduced passerines harboured greater viral diversity than endemic species, while social behaviour was a key predictor of virome composition with flocking species exhibiting higher viral richness and diversity than solitary or pair-living taxa. In contrast, non-viral microbial communities were primarily shaped by host species and diet, indicating that viral communities are influenced by ecological processes distinct from those associated with the non-viral microbiome. These findings provide new insight into the ecological and behavioural drivers of avian viral diversity.

microbiology↗

Spatial Transcriptomics Reveals Region-Specific Host Responses in Amoebic Gill Disease of Atlantic Salmon

Amoebic gill disease (AGD), caused by the parasite Neoparamoeba perurans, is a major welfare and economic burden for the Atlantic salmon aquaculture industry. However, the spatial organisation of immune functions within the gill, the site of infection, remains poorly resolved. Here, we present the first spatial transcriptomic atlas of the Atlantic salmon gill affected by AGD, generated using 10x Genomics Visium on four AGD-positive fish, confirmed by gill scoring and quantitative PCR for parasite load. As no uninfected gills were included, this study maps the anatomical and immunological organisation of AGD-affected gills rather than defining AGD-specific pathology. Unsupervised clustering of spatial gene expression resolved distinct transcriptional domains that grouped into four principal anatomical compartments of the gill, including (i) epithelial and lamellar regions defined by keratin and osmoregulatory gene expression, (ii) gill arch regions enriched for connective tissue and smooth muscle markers, (iii) an erythroid-associated vascular cluster, and (iv) a skeletal muscle cluster with signatures of glycolysis and oxidative phosphorylation. Across these domains, we identified a spatially organised and diffused immune landscape, with pattern recognition receptors, antimicrobial effectors and chemokines concentrated at the filament surface, and immunoglobulin light chain transcripts consistent with B lymphocyte activity enriched toward the gill arch. Integration of the spatial data with a published single-nucleus reference atlas using reference-based deconvolution resolved the cellular identity underlying these domains and revealed frequent co-localisation of immune and structural cell types, suggesting regulated cell to cell communication within the gill-associated lymphoid tissue. Overall, our results show that the Atlantic salmon gill is not a transcriptionally uniform surface but a regionally specialised organ, with immune functions distributed across, and specialised within, distinct anatomical compartments

immunology↗

Interactions between human milk components and infant polygenic risk predict childhood atopy

BackgroundAlthough human milk (HM) confers important health benefits, how bioactive milk components (e.g., microbiota, oligosaccharides, and fatty acids) interact with infant genetics to influence childhood atopy remains poorly understood. ObjectiveWe investigated interactions between infant genomic susceptibility and exposure to maternal human milk components (HMCs) and assessed whether integrating these genetic and milk features improves prediction of childhood atopy. MethodsLeveraging infant genomic and maternal HMC data from the CHILD Cohort Study, we conducted gene-milk interaction analysis using linear regression models that integrated polygenic risk scores (PRS) of nursing infants with multiple HMC types. Gradient-boosting machines (GBMs) were used to evaluate predictive performance of HMCs and infant PRS for childhood atopy. ResultsChildhood atopy was associated with interactions between infant genomics (e.g., PRS associated with atopy) and exposure to specific human milk microbes (e.g., Abiotrophia, PBonf=0.005, {beta}=0.29), as well as networks of co-occurring HMCs (e.g., a module containing Bifidobacterium longum, 2-fucosyllactose, and eicosapentaenoic acid, P=0.009, {beta}=-12.3). A GBM integrating HMCs and infant PRS achieved the highest predictive performance for childhood atopy with an area under the curve (AUC) of 0.78, outperforming models based on individual HMC types or PRS alone (AUC range: 0.54-0.63). ConclusionIntegration of maternal HMC exposures with infant genomics reveals interaction effects that contribute to prediction of childhood atopy. Understanding how early-life exposures such as HMCs impact the health of children differently depending on their genomic profiles may facilitate the development of personalized intervention strategies to reduce the burden of these health outcomes during childhood. Key messagesO_LIInteractions between infant polygenic risk and exposure to human milk components are associated with childhood atopy. C_LIO_LINetworks of co-occurring human milk microbiota, oligosaccharides, and fatty acids may influence childhood atopy, with effects varying by infant genomic susceptibility. C_LIO_LIIntegration of human milk components with infant genomics improves prediction of childhood atopy compared with individual milk components or genomics alone. C_LI Capsule SummaryThis study demonstrates that interactions between infant polygenic risk and maternal milk components improve prediction of childhood atopy, highlighting opportunities for personalized early-life prevention strategies.

genomics↗

Phosphoserine aminotransferase SerC is a central metabolic checkpoint and druggable vulnerability in Mycobacterium tuberculosis

Serine metabolism is fundamental to the pathogenicity of Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), yet its full metabolic scope and therapeutic potential remain unclear. Here we show that the phosphoserine aminotransferase serC is an essential metabolic node that coordinates central carbon and nitrogen flux and enables intracellular survival in the host. Deletion of serC caused severe growth defects across macrophage and murine infection models and rewired central carbon metabolism, reducing glycolytic, tricarboxylic-acid-cycle, and methylcitrate-cycle fluxes while altering one-carbon, branched-chain, and amino-acid biosynthetic pathways. Transposon sequencing identified sdaA-dependent serine deamination and the glycine cleavage system as key determinants of serine-based nitrogen assimilation, while revealing redundancy in serine transport. Our findings validate serine biosynthesis as a vulnerable, druggable metabolic target in Mtb and highlight it as a promising route for the development of urgently needed therapies against TB, which continues to kill millions of people each year.

microbiology↗

Feed Composition and Antibiotic Supplements Modulate Digestive Enzyme Activities and Alter Gut Microbiome of Pacific White Shrimp

The transition from fishmeal to sustainable alternatives in aquaculture is essential, however the physiological and microbial impacts of alternative diets in shrimp remain poorly understood. Here, we examine how substituting fishmeal with plant-based proteins such as guar and soybean meals, the inclusion of feather meal, and the use of a commonly used antibiotic (gentamicin) influence digestive enzyme function, protein digestibility, and gut microbial assemblages in Litopenaeus vannamei (Pacific white shrimp). The guar-based diet notably altered gut microbiota composition and decreased leucine aminopeptidase activity while maintaining high protein digestibility (>90%). In contrast, the soya/feather diet caused greater disruption to enzyme activity and microbial communities, resulting in reduced digestibility ([~]75%). The gent/guar diet showed comparable digestibility and microbial stability to the guar diet, with only minor shifts at the genus level. Although digestibility data for the acclimation diet were unavailable, these findings highlight diet-specific physiological and microbial responses to fishmeal substitutes. This emphasizes the need to consider dietary formulation, digestive function, and microbiome dynamics when developing sustainable aquafeeds for shrimp farming. ImportanceThe Pacific white shrimp (Litopenaeus vannamei) is a cornerstone of global aquaculture, yet optimizing its diet remains challenging. Current shrimp farming heavily depends on fishmeal, an unsustainable protein source, and antibiotic use to maintain shrimp health raises concerns about antimicrobial resistance and environmental impacts. This study highlights how alternative dietary formulations, including plant-based proteins and antibiotic supplements, influence shrimp digestive physiology and reshape gut microbiomes. Understanding these interactions is crucial to developing feed formulations that support robust shrimp growth and health without excessive reliance on antibiotics or fishmeal. By demonstrating how specific dietary ingredients affect both shrimp digestion and beneficial gut bacteria, this research provides valuable insights that can inform sustainable and responsible shrimp aquaculture practices globally.

microbiology↗

Understanding the Transfer and Persistence of Antimicrobial Resistance in Aquaculture Using a Model Teleost Gut System

The development, progression, and dissemination of antimicrobial resistance (AMR) is determined by interlinked human, animal, and environmental drivers, posing severe risks to human health. Conjugative plasmid transfer drives the rapid dissemination of AMR among bacteria. Besides antibiotic judicious use and implementation of antibiotic stewardship programs, mitigating antibiotic resistance spread requires an understanding of the dynamics of AMR transfer among microbial communities, as well as the role of various microbial taxa as potential reservoirs that promote long term AMR persistence. Here, we employed Hi-C, a high-throughput, culture-free technique, combined with qPCR, to monitor carriage and transfer of a multidrug-resistant plasmid within an Atlantic salmon in vitro gut model during florfenicol treatment, a benzenesulfonyl antibiotic widely deployed in fin-fish aquaculture. Microbial communities from the pyloric ceaca of three healthy adult farmed salmon were inoculated into three bioreactors developed for the SalmoSim gut system. The model system was then inoculated with an Escherichia coli strain ATCC 25922 carrying plasmid pM07-1 and treated with florfenicol at a concentration of 150 mg/L fish feed media for five days prior to a washout/recovery phase. Hi-C and metagenomic sequencing identified numerous transfer events, including to gram-negative and gram-positive taxa and, crucially, continuing transfer and persistence of the plasmid once florfenicol treatment had been withdrawn. Our findings highlight the role of commensal teleost gut flora as a reservoir for AMR, and our system provides a model to study how different treatment regimes and interventions may be deployed to mitigate AMR persistence.

microbiology↗

High resolution longitudinal molecular and morphological tracking of planktonic threats to salmon aquaculture.

Marine-phase salmonid aquaculture is a major component of the coastal economies of Northern Europe, North America and Chile and is under threat from numerous challenges to gill health, many of which originate from the phyto- and zooplankton. Associated losses are growing as a proportion of production year on year. A first step towards mitigating losses is to characterize the biological drivers of poor gill health. Numerous planktonic species have been implicated, including toxic and siliceous microalgae, hydrozoans and scyphozoans; however, rigorous longitudinal surveys of planktonic diversity and gill health have been lacking. In the current study, we present and assess an exhaustive identification approach combining both morphological and molecular methods (environmental DNA metabarcoding) approaches in combination with robust statistical models to identify the planktonic drivers of complex gill disease (CGD) and fish mortality. We undertook longitudinal molecular and microscopic evaluation at two marine aquaculture facilities on the west coast of Scotland using daily data collected during the 2021 growing season (March-October). Examining these two different sites, one sheltered and one exposed to the open sea, we identified new, important, and unexpected planktonic drivers (e.g. doliolids and appendicularians) of CGD and mortality and confirmed the significance of some established threats (e.g. hydrozoans and diatoms). We also explored delayed or lagged effects of planktonic abundances on gill health and undertook a comparison of environmental DNA metabarcoding and microscopy in their ability to identify and quantify planktonic species. Our data highlight the diversity of planktonic threats to salmonid aquaculture as well as the importance of using both molecular and morphological approaches to detect those. Despite our study relying on two farm sites only, our results evidence the role of the different planktonic players on salmon gill disease; there is now an urgent need to expand systematic longitudinal molecular and morphological approach across multiple sites and over multiple years. The resultant catalogue of main biological drivers will enable early warning systems, new treatments and, ultimately, a sustainable platform for future salmonid aquaculture in the marine environment.

zoology↗

Understanding the Mechanisms of Salmonella Typhimurium resistance to Cannabidiol

The emergence of multidrug resistance poses a huge risk to public health globally. Yet these recalcitrant pathogens continue to rise in incidence rate with resistance rates significantly outpacing the speed of antibiotic development. This therefore presents an aura of related health issues such as untreatable nosocomial infections arising from organ transplants, surgeries, as well as community acquired infections that are related to people with compromised immunity e.g., diabetic and HIV patients etc. There is a global effort to fight multidrug resistant pathogens spearheaded by the World Health Organization, thus calling for research into novel antimicrobials agents to fight multiple drug resistance. Previously, our laboratory demonstrated that Cannabidiol (CBD) was an effective antimicrobial against Salmonella Typhimurium (S. Typhimurium). However, we observed resistance development over time. To understand the mechanisms S. Typhimurium uses to develop resistance to Cannabidiol (CBD), we studied the abundance of bacteria lipopolysaccharide (LPS) and membrane sterols of both susceptible and resistant S. Typhimurium. Using real-time quantitative polymerase chain reaction (rt qPCR), we also analyzed the expression of selected genes known for aiding resistance development in S. Typhimurium. We discovered that there was a significantly higher expression of blaTEM, fimA, fimZ, and integrons in the CBD-resistant bacteria, and these were also accompanied by a shift in abundance in cell surface molecules such as lipopolysaccharide (LPS) and sterols.

microbiology↗

Gestational stress decreases postpartum mitochondrial respiration in the prefrontal cortex of female rats

Postpartum depression (PPD) is a major psychiatric complication of childbirth, affecting up to 20% of mothers, yet remains understudied. Mitochondria, dynamic organelles crucial for cell homeostasis and energy production, share links with many of the proposed mechanisms underlying PPD pathology. Brain mitochondrial function is affected by stress, a major risk factor for development of PPD, and is linked to anxiety-like and social behaviors. Considering the importance of mitochondria in regulating brain function and behavior, we hypothesized that mitochondrial dysfunction is associated with behavioral alterations in a chronic stress-induced rat model of PPD. Using a validated and translationally relevant chronic mild unpredictable stress paradigm during late gestation, we induced PPD-relevant behaviors in adult postpartum Wistar rats. In the mid-postpartum, we measured mitochondrial function in the prefrontal cortex (PFC) and nucleus accumbens (NAc) using high-resolution respirometry. We then measured protein expression of mitochondrial complex proteins and 4-hydroxynonenal (a marker of oxidative stress), and Th1/Th2 cytokine levels in PFC and plasma. We report novel findings that gestational stress decreased mitochondrial function in the PFC, but not the NAc of postpartum dams. However, in groups controlling for the effects of either stress or parity alone, no differences in mitochondrial respiration measured in either brain regions were observed compared to nulliparous controls. This decrease in PFC mitochondrial function in stressed dams was accompanied by negative behavioral consequences in the postpartum, complex-I specific deficits in protein expression, and increased Tumor Necrosis Factor alpha cytokine levels in plasma and PFC. Overall, we report an association between PFC mitochondrial respiration, PPD-relevant behaviors, and inflammation following gestational stress, highlighting a potential role for mitochondrial function in postpartum health.

neuroscience↗

Optimization of universal primer set for the identification of all Influenza A viruses using real-time PCR

Avian Influenza Virus (AIV) occurs worldwide among aquatic wild and may mutate into a strain capable of efficient human-to-human transmission and cause a pandemic that could kill a large fraction of the human population. The purpose of this study is to efficiently identify and diagnose the virus for immediate treatment and prevention. Real-Time Reverse Transcription-Polymerase Chain Reaction (RRT-PCR or qPCR) was identified as the most efficient way to detect AIV in previous laboratory research, however only one pair of primers was used. In order to further optimize the test and make it commercially available in the future, we first tested an eight pair primer set via RRT-PCR by using standard AIV isolates from Dr.Gaimbrones lab (Auburn University). Using the AIV isolates, the optimal cDNA and primer concentrations were determined, this aided in the identification of the most sensitive primer set. Primers PA, HA, NP, and NA were able to detect the cDNA of positive AIV isolates at a low concentration of 0.0039 mg/ml. AIV cDNA were detected by primers M and HA at its lowest concentration of 0.0001 and 0.01 pmol/l. In order to further test our lab results, 20 fecal samples from aquatic wild birds were collected from Alabama Shakespeare Park located in Montgomery, Alabama during the winter season. The samples were analyzed using RRT-PCR. HA primer set detected 10 positive samples for Avian Influenza and is the most sensitive primer set to be used in RRT-PCR. The field sample detection confirmed laboratory results and revealed that local aquatic birds are actively shedding low pathogenic avian influenza virus(LPAIV). The optimization of all primer sets used in this study will aid in disease surveillance, facilitate quick diagnosis of Influenza A viruses, and implement an effective prevention of flu pandemic.

microbiology↗

In silico Elucidation of Dihydroquinine Mechanism of Action against Toxoplasma gondii

Dihydroquinine (DHQ), is a quinine-based compound with anti-malarial properties. However, little is known about its mechanism of action against T. gondii inhibition, which shares similar biology with Plasmodium spp. In order to explore DHQ activity as an inhibitor of T. gondii using in vitro assays, we first used an in silico approach to decipher its mechanisms of action based on previous knowledge about its disruption of nucleic acid and protein synthesis. An in silico study was performed on T. gondii parasite replication, transcriptional and translational machinery to decipher the binding potentials of DHQ to some top selected enzymes. We report for the first time, using an in silico analysis that showed that DHQ binds strongly to DNA gyrase, Calcium Dependent Protein Kinase 1 (CDPK 1), and prolyl tRNA synthetase and thus could affect DNA replication, transcriptional and translational activities in T. gondii. Also, we found DHQ to effectively bind to mitochondria detoxifying enzymes (i.e., superoxide dismutase (SOD), peroxidoxin, and Catalase (CAT)). In conclusion, DHQ could be a lead compound for the treatment of toxoplasmosis when successfully evaluated using in vitro and in vivo models to confirm its effectiveness and safety.

cell biology↗

Lipid mediated inhibition of Niemann-Pick C1 protein is an evolutionary conserved feature of multiple Mycobacterium lineages and non-tubercular mycobacteria.

Mycobacterium tuberculosis (Mtb) is the causative agent of tuberculosis (TB) and is a major cause of human morbidity and mortality. Crucially, Mtb can persist and replicate within host macrophages (M[FE]) and subvert multiple antimicrobial defense mechanisms. How this is achieved is incompletely understood. Previously, we reported that lipids shed by persistent mycobacteria inhibit NPC1, the lysosomal protein deficient in most cases of the rare, inherited lysosomal storage disorder Niemann-Pick disease type C (NPC). Inhibition of NPC1 leads to a drop in lysosomal calcium levels blocking phagosome-lysosome fusion and thereby leads to mycobacterial persistence. Studies of mycobacterial lineages have identified events during mycobacterial evolution that result in the acquisition of persistence. We speculated that the production of specific cell wall lipid(s) capable of inhibiting NPC1 activities could have been a critical step in the evolution of pathogenicity. In this study, we have therefore investigated whether lipid extracts from clinical Mtb strains representative of multiple Mtb lineages, members of the Mtb complex (MTBC) and selected non-tubercular mycobacteria (NTM) inhibit the NPC pathway. We have found that the ability to inhibit the NPC pathway was present in all clinical isolates studied from Mtb lineages 1, 2 and 4. We also found that lipids from MTBC member, Mycobacterium bovis and the NTM, Mycobacterium abscessus and Mycobacterium avium also inhibited the NPC pathway. However, when lipids were assayed from Mycobacterium canettii (M. canettii), a smooth tubercle mycobacterium, which is considered to resemble the common ancestor of the MTBC no inhibition of the NPC1 pathway was detected. We therefore conclude that the evolution of mycobacterial cell wall lipids that inhibit the NPC pathway evolved early and post divergence from M. canettii related mycobacteria and NPC1 inhibition significantly contributes to the ability of these pathogens to persist and cause disease. Authors summaryMycobacterium tuberculosis (Mtb) actively modifies the hostile intracellular environment of host cells to create a niche in which it can persist and replicate. How this is accomplished is incompletely understood. We previously reported an unexpected phenotypic similarity between cells infected with pathogenic mycobacteria and those of the rare, neurodegenerative lysosomal storage disorder, Niemann-Pick disease type C (NPC). Mechanistically, we showed that pathogenic mycobacteria shed lipids that inhibit NCP1, the lysosomal membrane protein that is dysfunctional in NPC and thereby establish conditions that favour their survival. In this study, we have investigated the phylogenetic distribution of lipids that inhibit NPC1. We have screened lipid extracts from multiple clinical mycobacterial isolates representing different Mtb lineages, other members of the Mtb complex and non-tuberculous mycobacteria for their ability to induce NPC phenotypes. We detected activity in all of the groups tested, but not from Mycobacterium canettii, which is believed to resemble the ancestral species. These data indicate that targeting of NPC1 to achieve intracellular persistence evolved early in the evolution of the Mtb complex, but after divergence from the presumed ancestral species.

microbiology↗

ExSTED microscopy reveals contrasting functions of dopamine and somatostatin CSF-c neurons along the central canal

The spatial location of cerebrospinal fluid contacting (CSF-c) neurons enables important regulatory homeostatic functions regarding pH and motion control. Their intricate organization, facing the central canal and extending across the spinal cord, in relation to specific subtypes is poorly understood. This calls for imaging methods with a high spatial resolution (5-10 nm) to resolve the synaptic and ciliary compartments of each individual cell to elucidate their signalling pathways and enough throughput to dissect the cellular organization. Here, light-sheet and expansion microscopy resolved the persistent ventral and lateral organization of dopamine and somatostatin CSF-c neuronal types. The number of somatostatin-containing dense core vesicles, resolved by STED microscopy, was shown to be markedly reduced upon each exposure to alkaline or acidic pH inhibiting any movement as part of a homeostatic response. Their cilia symmetry was unravelled by ExSTED as sensory in contrast with the motile one found in the dopaminergic ph insensitive neurons. This novel experimental workflow elucidates the functional role of CSF-c neuron subtypes in situ paving the way for further spatial and functional cell type classification.

neuroscience↗

High mannose N-glycans on red blood cells as phagocytic ligands, mediating both sickle cell anaemia and resistance to malaria

In both sickle cell disease (SCD) and malaria, red blood cells (RBCs) are phagocytosed in the spleen, but receptor-ligand pairs mediating uptake have not been identified. Here, we report that patches of high mannose N-glycans (Man5-9GlcNAc2), expressed on diseased or oxidized RBC surfaces, bind the mannose receptor (CD206) on phagocytes to mediate clearance. Extravascular haemolysis in SCD correlates with high mannose glycan levels on RBCs. Infection of RBCs with Plasmodium falciparum expose surface mannose N-glycans on healthy RBCs, which occurred at significantly higher levels on RBCs from subjects with sickle cell trait compared to those lacking haemoglobin S. The glycans were associated with high molecular weight complexes and protease-resistant, lower molecular weight fragments containing spectrin. Recognition of surface N-linked high mannose glycans, a novel response to cellular stress, is the first molecular mechanism common to both the pathogenesis of SCD and resistance to severe malaria in sickle cell trait.

immunology↗

Gene-tree Species-tree Discordance in the Eared Seals is best explained by Incomplete Lineage Sorting following Explosive Radiation in the Southern Hemisphere

AO_SCPLOWBSTRACTC_SCPLOWThe phylogeny and systematics of fur seals and sea lions (Otariidae) have long been studied with diverse data types, including an increasing amount of molecular data. However, only a few phylogenetic relationships have reached acceptance because of strong gene-tree species tree discordance. Divergence times estimates in the group also vary largely between studies. These uncertainties impeded the understanding of the biogeographical history of the group, such as when and how trans-equatorial dispersal and subsequent speciation events occurred. Here we used high-coverage genome-wide sequencing for 14 of the 15 species of Otariidae to elucidate the phylogeny of the family and its bearing on the taxonomy and biogeographical history. Despite extreme topological discordance among gene trees, we found a fully supported species tree that agrees with the few well-accepted relationships and establishes monophyly of the genus Arctocephalus. Our data support a relatively recent trans-hemispheric dispersal at the base of a southern clade, which rapidly diversified into six major lineages between 3 to 2.5 Ma. Otaria diverged first, followed by Phocarctos and then four major lineages within Arctocephalus. However, we found Zalophus to be non-monophyletic, with California (Z. californianus) and Steller sea lions (Eumetopias jubatus) grouping closer than the Galapagos sea lion (Z. wollebaeki) with evidence for introgression between the two genera. Overall, the high degree of genealogical discordance was best explained by incomplete lineage sorting resulting from quasi-simultaneous speciation within the southern clade with introgresssion playing a subordinate role in explaining the incongruence among and within prior phylogenetic studies of the family.

evolutionary biology↗

Recent demographic histories and genetic diversity across pinnipeds are shaped by anthropogenic interactions and mediated by ecology and life-history

A central paradigm in conservation biology is that population bottlenecks reduce genetic diversity and negatively impact population viability and adaptive potential. In an era of unprecedented biodiversity loss and climate change, understanding both the determinants and consequences of bottlenecks in wild populations is therefore an increasingly important challenge. However, as most studies have focused on single species, the multitude of potential drivers and the consequences of bottlenecks remain elusive. Here, we used a comparative approach by integrating genetic data from over 11,000 individuals of 30 pinniped species with demographic, ecological and life history data to elucidate the consequences of large-scale commercial exploitation by 18th and 19th century sealers. We show that around one third of these species exhibit strong genetic signatures of recent population declines, with estimated bottleneck effective population sizes reflecting just a few tens of surviving individuals in the most extreme cases. Bottleneck strength was strongly associated with both breeding habitat and mating system variation, and together with global abundance explained a large proportion of the variation in genetic diversity across species. Overall, there was no relationship between bottleneck intensity and IUCN status, although three of the four most heavily bottlenecked species are currently endangered. Our study reveals an unforeseen interplay between anthropogenic exploitation, ecology, life history and demographic declines, sheds new light on the determinants of genetic diversity, and is consistent with the notion that both genetic and demographic factors influence population viability.

evolutionary biology↗