Biology subjects

King, E.

Publications and source records attributed to King, E..

At least 19 recordsLinked to original sources

bioRxiv2026

Twenty-five new microsporidian genomes: Insights into ploidy, reproduction, and the group's pangenome

Microsporidia are single-celled, obligately intracellular eukaryotic parasites of growing importance. Many aspects of their biology remain enigmatic, partly because of difficulties in sampling, culturing, and experimentally manipulating them. Here, we continue efforts to generate microsporidian genomes from serendipitously infected organisms sequenced for biodiversity genomics initiatives, such as the Darwin Tree of Life Project. We present 25 new microsporidian genomes: 14 biologically complete, including several at (near-)chromosome level, and 11 partial. Using RNA-seq data for three published genomes we identify Prokka as a suitable ab initio annotation approach for Microsporidia. Consistently annotating all available genomes, we investigate gene-content diversity across microsporidian clades. We find that the microsporidian pangenome exhibits extreme diversity, and that current genomic data substantially undersample the group's proteome space. Neither GC content nor genome span consistently explains orthogroup number across lineages, suggesting different evolutionary pressures. We find few one-to-one orthogroups in Microsporidia, as well as few orthogroups that are both lineage-specific and conserved across most species within a given lineage. Finally, Hi-C data confirm that tetraploid Amblyosporida microsporidia occur as two equivalent diploid units. In contrast, one Enterocytozoonida tetraploid genome suggests that all four genome copies occur within a single nucleus (a 'monokaryon'), confirming a previous proposal.

genomics↗

bioRxiv2026

Single-cell multiomic mapping of genetic predisposition to childhood B-cell acute lymphoblastic leukemia

Inherited genetic variation substantially increases the risk for developing childhood B-cell acute lymphoblastic leukemia (B-ALL), the most common cancer in children, yet the underlying mechanisms remain poorly understood. To address this limitation, we employ a single-cell multiomic framework to functionally dissect common regulatory variants associated with B-ALL risk. Coupling this multiomic analysis with assessment of allelic skews in chromatin accessibility, we reveal the impact of risk alleles and disruptions in transcription factor networks specific to B-cell progenitors, thereby providing mechanistic insights into altered regulatory programs underlying B-ALL predisposition. By constructing long-range variant-to-target gene maps, we identify 34 high-confidence B-ALL susceptibility genes. Among these, we uncover and functionally validate a risk allele that selectively upregulates expression of ELK3, a previously unrecognized regulator of B-cell development and leukemogenesis. Together, these findings establish a comprehensive variant-to-function map of cell state-specific regulatory disruptions underlying inherited predisposition to B-ALL and define new risk mechanisms, which could pave the way for future targeted prevention approaches.

cancer biology↗

bioRxiv2026

Cohesin loading at regulatory elements shapes 3D genome folding during erythropoiesis

During erythropoiesis, differentiating cells silence much of the genome while maintaining high expression of select genes. It remains unclear whether this transcriptional specialization is linked to specific changes in 3D genome organization. We generated deep Micro-C maps across human erythropoiesis and identified erythroid cis-regulatory elements (CREs) that function as "matchmakers" by strengthening loops between neighboring elements. Matchmakers are associated with high H3K4me1, increase in strength during differentiation, and are linked to the expression of key erythropoiesis genes. Simulations suggest that a moderate cohesin loading bias across broad enhancer regions can explain the features of matchmakers, particularly under chromatin compaction. Targeted transcription factor and cohesin perturbations reduced matchmaker-associated structures and gene expression. We propose that matchmakers represent a subset of CREs that concentrate loop extrusion near key genes during erythroid differentiation.

genomics↗

bioRxiv2026

Reference-free compound identification using computational prediction of molecular properties and multi-dimensional spectrometric measurements: a fentanyl case study

Mass spectrometry is used to identify chemicals to which humans are exposed, but it cannot directly determine molecular structures. Instead, structures are inferred by matching experimental spectra to libraries of spectra constructed from analyses of pure reference compounds. However, the chemical space of human exposures far exceeds the amount of experimental library spectra. Here, we evaluate a reference-free strategy for confident identification of unknown molecules. Using fentanyl as a case study, we created a suspect library of over 1 billion computationally predicted fentanyl analogs and predicted molecular properties through machine learning, molecular dynamics, and density functional theory. Multi-dimensional spectra from a blinded analysis of a mock fentanyl tablet were matched with the predicted library, yielding an average of three candidate structures per measured analog, with six exact identifications. This work emphasizes the promise of reference-free molecular measurements for assessing human exposure by merging computational predictions with high-dimensional measurements.

scientific communication and education↗

bioRxiv2026

Modeling mitochondrial inheritance enables high-precision single-cell lineage tracing in humans

Somatic mutations in mitochondrial DNA (mtDNA) provide natural barcodes that enable engineering-free lineage tracing in human tissues, but the complex dynamics of mtDNA inheritance across cell divisions and incomplete sampling of mtDNA introduce uncertainty in reconstructed lineages. Here, we present MitoDrift, a probabilistic framework that integrates Wright-Fisher drift dynamics with sparse single-cell measurements to produce confidence-refined lineage trees enriched for accurate clonal relationships. Validation with gold-standard lentiviral barcoding and whole-genome sequencing demonstrates that MitoDrift outperforms existing tree reconstruction methods in precision while maintaining high clonal recovery, enabling robust analyses linking lineage to cell state. Applying MitoDrift to human hematopoiesis reveals an age-associated decline in clonal diversity with differential impact across cell types and identifies heritable regulatory programs in hematopoietic stem cells in vivo, linking AP-1/stress-associated programs to clonal expansions. In multiple myeloma, MitoDrift captures therapy-associated clonal remodeling undetectable by copy number analysis, revealing phenotypic transitions and linking gene regulatory programs to differential drug sensitivity. Collectively, MitoDrift enables high-precision lineage tracing at scale and establishes quantitative lineage-state analysis in primary human tissues, linking clonal history to transcriptional and epigenetic programs in tissue homeostasis, aging, and disease.

genomics↗

bioRxiv2026

The genome of an enigmatic sea urchin parasite Echinomermella matsi Jones & Hagen, 1987 resolves its place among other invertebrate parasitic nematodes

We present a genome of Echinomermella matsi (Nematoda: Plectida: Benthimermithidae), a body cavity parasite of the green sea urchin Strongylocentrotus spp. commonly found along the coast of Central and Northern Norway. Three assemblies were generated, one from multiple individuals using Oxford Nanopore long read data and two from two individuals using PacBio long read data. The genome of Echinomermella matsi is 65 Mb long consisting of 7 chromosomes, with nematode Benchmarking Using Single Copy Orthologue (BUSCO) completeness reaching 61%. The E. matsi chromosome complement corresponds to the proposed Rhabditida ancestral linkage groups. Phylogenetic analyses using newly generated 18S rRNA genes and a multigene dataset consisting of BUSCO protein coding genes, supported by morphological observations of juveniles, firmly place Echinomermella within the nematode order Plectida, alongside nematode parasitoids of marine invertebrates, Trophomera or Neocamacolaimus. As a result, the generally free-living order Plectida includes at least three independently evolved lineages of nematodes symbiotic with various groups of aquatic and terrestrial invertebrates and with unicellular organisms. This, and the fact that Plectida is the closest sister lineage to Rhabditida as a whole, and one node away from the exclusively animal parasitic Spirurina, makes this lineage a valuable model for study of evolution of animal parasitism in the aquatic environment. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=115 SRC="FIGDIR/small/699767v1_ufig1.gif" ALT="Figure 1"> View larger version (38K): org.highwire.dtl.DTLVardef@d44b08org.highwire.dtl.DTLVardef@18a3310org.highwire.dtl.DTLVardef@1e79dforg.highwire.dtl.DTLVardef@d33b3b_HPS_FORMAT_FIGEXP M_FIG C_FIG Article summaryThe researchers generated a genome of Echinomermella matsi, a body cavity parasite of the green sea urchin, using PacBio and Oxford Nanopore long read sequencing. The genome is 65 Mb long, shows 61% of nematode BUSCO completeness, and consists of 7 chromosomes. Single and multiple gene phylogenies place Echinomermella within mostly free-living Plectida as one of the three independently evolved parasitic lineages. The authors suggest Echinomermella to be a valuable model to study evolution of animal parasitism in the aquatic environment. The genome can be used to develop biocontrol strategies of Echinomermella in mariculture of green sea urchin.

genomics↗

bioRxiv2026

Identification of novel inhibitors of Mycobacterium smegmatis growth through genome-wide overexpression of Cluster P3 mycobacteriophage Xavia genes

We examined whether genes encoded by the mycobacteriophage Xavia disrupt growth of Mycobacterium smegmatis, a widely used mycobacterial model. Seventy-one Xavia genes were individually expressed using an inducible plasmid system and assessed for effects on colony formation. Two genes were lethal even without induction, indicating toxicity under basal expression. Induction of sixteen additional genes reduced bacterial growth, spanning structural proteins, lysogeny regulators, DNA-associated enzymes, a lysis protein, and several genes with no known function. These findings expand functional insights into mycobacteriophage gene repertoires and identify candidates for future mechanistic studies. AbstractBacteriophage genomes encode large numbers of genes with no known function, and many of these genes affect essential host processes when expressed in a heterologous system. For mycobacteriophages, genome-wide overexpression in Mycobacterium smegmatis provides a direct way to identify proteins that impair growth and to determine which mycobacterial pathways are sensitive to phage gene products. To evaluate the cytotoxic potential of the Cluster P3 phage Xavia, a lineage that has not undergone functional screening, we constructed an arrayed pExTra library containing 71 predicted Xavia genes under control of the anhydrotetracycline inducible promoter pTet. All constructs were sequence-verified and transformed into M. smegmatis, and induction allowed measurement of gene-specific effects on growth. Two genes prevented recovery of transformants, suggesting toxicity under basal promoter leakiness. Inducible expression of 16 additional genes impaired growth, and these inhibitory proteins include structural components, regulators of lysogeny, enzymes of DNA metabolism, a lysis factor, and several proteins with no known function. Four of the strongest inhibitors were genes with no known function. These results extend functional screening into the previously untested P3 branch of Actinobacteriophages and identify new proteins that require mechanistic analysis.

microbiology↗

bioRxiv2025

Reprogramming the Rossmann Fold Signature Motif Creates Orthogonal Redox Biocatalysts

Biological reducing power is carried by nicotinamide adenine dinucleotide (phosphate) (NAD(P)/H), which supports cellular functions and cannot be specifically directed to engineered metabolic pathways. Nicotinamide mononucleotide (NMN(H)) has emerged as an orthogonal redox cofactor to address this challenge, yet strategies remain elusive for creating NMN(H)-specific enzymes that no longer interact with the cellular NAD(P)/H pools. Previous designs avoided perturbing the most ancient and conserved GxGxxG motif in Rossmann fold enzymes, the root cause of persistent NAD(P)/H recognition. Herein, we demonstrated that this motif, though long considered essential, is in fact mutable to yield active NMN+-specific enzymes. This is implemented on two unrelated model enzymes chosen to garner orthogonal reducing power from either the cheap electron source phosphite or glycolysis. On phosphite dehydrogenase (PTDH), variants NRC-01 and NRC-02 eliminated electron leaking to numerous NAD(P)H-dependent side reactions in whole cells and crude cell lysates while driving NMNH-dependent biotransformation with [~]240-fold higher productivity than existing catalysts. On glyceraldehyde-3-phosphate dehydrogenase (GapA), variant RSQ featured a [~]2.9x104-fold cofactor specificity switch to NMN+ from NAD+. Combined Rosetta modeling, systematic structural alignment, and experimental results revealed that Rossmann fold reprogramming, paired with engineered structural reinforcement, may offer a general route to orthogonal redox biocatalysts.

molecular biology↗

bioRxiv2025

Engineering the key central metabolic enzyme to utilize a non-canonical redox cofactor

Redesigning central metabolism enzymes to utilize non-canonical cofactors that are orthogonal to NAD+ and NADP+ may allow partitioning of reducing power into a distinct redox cofactor pool that is preserved for user-desired biosynthetic tasks, without being dissipated by the complex natural metabolism in the cells. Here, we engineer Escherichia coli glyceraldehyde-3-phosphate dehydrogenase (GapA), the key enzyme in glycolysis, to utilize nicotinamide mononucleotide (NMN+) while greatly reducing its original activity with its native cofactor, NAD+. Through rational design, we identify the variant A180S with a [~]3-fold increase in NMN+ specific activity compared to that of the wildtype (WT). Next, we design a double mutant, G10R-A180S (RS), where G10R mutation hampers the catalytic efficiency for NAD+ but also decreased the activity toward NMN+. Importantly, based on the hypothesis that the role of NAD+ in coordinating oligomer interface must be recapitulated in NMN+-utilizing enzymes, we develop a triple mutant G10R-A180S-G187Q (RSQ). Rosetta modeling predicts that the new mutation G187Q bridges separate subunits across the cofactor binding pocket, which possibly affords stronger association of the GapA tetramer, the active form of this enzyme. This final GapA variant features a [~]2.8 x 104 switch of cofactor specificity from GapAs natural cofactor NAD+ to the non-canonical cofactor NMN+. Overall, this work demonstrates the engineering of a highly conserved, central metabolic enzyme for the utilization of a non-canonical redox cofactor NMN+. The design principle discovered here may be broadly applicable to many enzymes that bind cofactors using an intersubunit pocket.

molecular biology↗

bioRxiv2025

High-risk clonal groups of Avian Pathogenic Escherichia coli (APEC) demonstrate heterogeneous phenotypic characteristics in vitro and in vivo

Avian Pathogenic Escherichia coli (APEC), a major bacterial pathogen of poultry, is comprised of a diverse range of high-risk clonal groups. However, phenotypic interactions with the avian host cell and how they may differ between lineages remains poorly understood. Therefore, the ability of predominant and outbreak-associated APEC clonal groups to invade and survive within avian host cells, as well as virulence within the Galleria mellonella infection model was investigated. The molecular characterisation of APEC isolated from an outbreak of colibacillosis in turkey poults in the UK, identified APEC sequence type (ST)-101 as the dominant clonal group, carrying a high number of virulence factors. As such, ST-101 was compared as an outbreak-associated lineage to a range of predominant APEC high-risk clonal groups (ST-23, ST-140, ST-95, ST-117). Utilising in vitro cell culture models, APEC isolates displayed comparable adhesion to 8E11 chicken epithelial gut and HD11 chicken macrophage cell lines. However, a trend of increased invasion of the 8E11 cells, and intracellular survival within HD11 macrophages was observed for ST-95, ST-101, and ST-140 APEC, relative to ST-23 and ST-117, suggestive of pronounced phenotypic differences between clonal groups. However, in HD11 cell assays, no difference in magnitude of elicited immune response was observed between lineages, indicating lineages had differing capacities to resist phagocyte killing. In vivo virulence in the Galleria mellonella infection model was also observed to differ between APEC genotypes, with ST-117 inducing the highest mortality, despite the comparatively lower epithelial invasion and intramacrophage survival to other lineages. Collectively, this suggests a distinct phenotypic profile associated with high-risk clonal groups within APEC, potentially allowing the future development of broad-spectrum disease management strategies.

microbiology↗

bioRxiv2024

Multi-laboratory Study Establishes Reproducible Methods for Plant-Microbiome Research in Fabricated Ecosystems

Inter-laboratory replicability is crucial yet challenging in microbiome research. Leveraging microbiomes to promote soil health and plant growth requires understanding underlying molecular mechanisms using reproducible experimental systems. In a global collaborative effort involving five laboratories, we aimed to help advance reproducibility in microbiome studies by testing our ability to replicate synthetic community assembly experiments. Our study compared fabricated ecosystems constructed using two different synthetic bacterial communities, the model grass Brachypodium distachyon, and sterile EcoFAB 2.0 devices. All participating laboratories observed consistent inoculum-dependent changes in plant phenotype, root exudate composition, and final bacterial community structure where Paraburkholderia sp. OAS925 could dramatically shift microbiome composition. Comparative genomics and exudate utilization linked the pH-dependent colonization ability of Paraburkholderia, which was further confirmed with motility assays. The study provides detailed protocols, benchmarking datasets, and best practices to help advance replicable science and inform future multi-laboratory reproducibility studies.

microbiology↗

bioRxiv2024

Transcription factor networks disproportionately enrich for heritability of blood cell phenotypes

Most phenotype-associated genetic variants map to non-coding regulatory regions of the human genome. Moreover, variants associated with blood cell phenotypes are enriched in regulatory regions active during hematopoiesis. To systematically explore the nature of these regions, we developed a highly efficient strategy, Perturb-multiome, that makes it possible to simultaneously profile both chromatin accessibility and gene expression in single cells with CRISPR-mediated perturbation of a range of master transcription factors (TFs). This approach allowed us to examine the connection between TFs, accessible regions, and gene expression across the genome throughout hematopoietic differentiation. We discovered that variants within the TF-sensitive accessible chromatin regions, while representing less than 0.3% of the genome, show a [~]100-fold enrichment in heritability across certain blood cell phenotypes; this enrichment is strikingly higher than for other accessible chromatin regions. Our approach facilitates large-scale mechanistic understanding of phenotype-associated genetic variants by connecting key cis-regulatory elements and their target genes within gene regulatory networks.

genomics↗

bioRxiv2024

Species-specific interactions with apex carnivores yield unique benefits and burdens for mesocarnivores

Mesocarnivores navigate a complex risk-reward continuum in ecosystems shared with their apex counterparts, balancing scavenging opportunities with risks of mortality. However, the risks to mesocarnivores in multi-carnivore systems are not uniform--often varying with specific apex-meso pairings. Using camera traps and GPS-telemetry, we examined space-use, temporal activity, fine-scale interactions, and scavenging behavior of apex (wolves, cougars) and mesocarnivores (red foxes, coyotes) in northern Yellowstone National Park, USA. Coyote space use was positively linked to wolf presence, while red fox space use was positively linked to cougar presence. Notably, photo-detection rates of mesocarnivores doubled within 24 hours of apex carnivore detections--except for coyotes following cougars. Coyotes were more frequent scavengers at wolf and cougar kills than red foxes, but they also suffered the highest mortality rates. Over 60% of wolf caused coyote mortalities were linked to wolf kill-sites, though wolves rarely consumed the coyotes themselves. In contrast, cougars hunted and consumed coyotes as prey, posing an additional risk of predation. These findings highlight how divergent hunting strategies and habitat preferences between canid and felid apex carnivores create separate risks for mesocarnivores. Our study offers new insights into the species-specific behavioral dynamics that can shape trophic interactions in multi-carnivore systems.

ecology↗

bioRxiv2024

Skeletal Muscle Specific PolG Dysfunction Activates the Integrated Stress Response and Promotes a Cachexia like Phenotype

During mitochondrial damage, information is relayed between the mitochondria and nucleus to coordinate precise responses to preserve cellular health. One such pathway is the mitochondrial integrated stress response (mtISR), which is specifically activated by mitochondrial DNA (mtDNA) damage. However, the causal molecular signals responsible for this activation remain elusive. A gene often associated with mtDNA mutations/deletions is Polg1, which encodes the mitochondrial DNA Polymerase {gamma} (PolG). Here, we describe what is to our knowledge the first conditional muscle specific model of PolG mutation, and demonstrate a rapid development of mitochondrial dysfunction and cachexia in these animals from [~]5 months of age. Detailed molecular profiling of muscles demonstrated robust activation of the mtISR, likely mediated upstream by the HRI/DELE1 stress pathway. This was accompanied by striking alterations to the mitochondrial folate cycle and its metabolites, strongly implying imbalanced folate intermediates as a previously unrecognised pathology driving the mtISR in mitochondrial disease.

physiology↗

bioRxiv2024

The endophytic fungus Serendipita indica alters auxin distribution in Arabidopsis thaliana roots through alteration of auxin transport and conjugation to promote plant growth

Plants share their habitats with a multitude of different microbes. This close vicinity promoted the evolution of inter-organismic interactions between plants and many different microorganisms that provide mutual growth benefits both to the plant and the microbial partner. The symbiosis of Arabidopsis thaliana with the beneficial root colonizing endophyte Serendipita indica represents a well-studied system. Co-colonization of Arabidopsis roots with S. indica significantly promotes plant growth. Due to the notable phenotypic alterations of fungus-infected root systems, the involvement of a reprogramming of plant hormone levels, especially that of indole-3-acetic acid, has been suggested earlier. However, until now, the molecular mechanism by which S. indica promotes plant growth remains largely unknown. This study used comprehensive transcriptomics, metabolomics, reverse genetics, and life cell imaging to reveal the intricacies of auxin-related processes that affect root growth in the symbiosis between A. thaliana and S. indica. Our experiments revealed the essential role of tightly controlled auxin conjugation in the plant-fungus interaction. It particularly highlighted the importance of two GRETCHEN HAGEN 3 (GH3) genes, GH3.5 and GH3.17, for the fungus infection-triggered stimulation of biomass production, thus broadening our knowledge about the function of GH3s in plants. Furthermore, we provide evidence for the transcriptional alteration of the PIN2 auxin transporter gene in roots of Arabidopsis seedlings infected with S. indica and demonstrate that this transcriptional adjustment affects auxin signaling in roots, which results in increased plant growth.

plant biology↗

bioRxiv2023

Revisiting Hox gene evolution and Hox clusterlinkage across Nematoda

Hox genes are central to metazoan body plan formation, patterning and evolution, playing a critical role in cell fate decisions early in embryonic development in invertebrates and vertebrates. While the archetypical Hox gene cluster consists of members of nine ortholog groups (HOX1-HOX9), arrayed in close linkage in the order in which they have their anterior-posterior patterning effects, nematode Hox gene sets do not fit this model. The Caenorhabditis elegans Hox gene set is not clustered and contains only six Hox genes from four of the ancestral groups. The pattern observed in C. elegans is not typical of the phylum, and variation in orthologue set presence and absence and in genomic organisation has been reported. Recent advances in genome sequencing have resulted in the availability of many novel genome assemblies in Nematoda, especially from taxonomic groups that had not been analysed previously. Here, we explored Hox gene complements in high-quality genomes of 80 species from all major clades of Nematoda to understand the evolution of this key set of body pattern genes and especially to probe the origins of the "dispersed" cluster observed in C. elegans. We also included the recently available high-quality genomes of some Nematomorpha as an outgroup. We find that nematodes can have Hox genes from up to six orthology groups. While nematode Hox "clusters" are often interrupted by unrelated genes we identify species in which the cluster is intact and not dispersed.

developmental biology↗

bioRxiv2023

Shifting Redox Reaction Equilibria on Demand Using an Orthogonal Redox Cofactor

Natural metabolism relies on chemical compartmentalization of two redox cofactors, NAD+ and NADP+, to orchestrate life-essential redox reaction directions. However, in whole cells the reliance on these canonical cofactors limits flexible control of redox reaction direction as these reactions are permanently tied to catabolism or anabolism. In cell-free systems, NADP+ is too expensive in large scale. We have previously reported the use of nicotinamide mononucleotide, (NMN+) as a low-cost, noncanonical redox cofactor capable of specific electron delivery to diverse chemistries. Here, we present Nox Ortho, an NMNH-specific water-forming oxidase, that completes the toolkit to modulate NMNH/NMN+ ratio. This work uncovers an enzyme design principle that succeeds in parallel engineering of six butanediol dehydrogenases as NMN(H)-orthogonal biocatalysts consistently with a 103 - 106 -fold cofactor specificity switch from NAD(P)+ to NMN+. We combine these to produce chiral-pure 2,3-butanediol (Bdo) isomers without interference from NAD(H) or NADP(H) in vitro and in E. coli cells. We establish that NMN(H) can be held at a distinct redox ratio on demand, decoupled from both NAD(H) and NADP(H) redox ratios in vitro and in vivo.

synthetic biology↗

bioRxiv2023

The Lion's Share: Implications of carnivore diet on endangered herbivores in Tsavo

Predation by mammalian carnivores can have cascading, regulatory effects across ecological communities. An understanding of predator diet can therefore provide crucial information regarding their ecology and conservation, as well as their impacts on prey populations. Using scats collected between 2019 and 2023, coupled with estimates of prey abundance from aerial surveys, we characterized lion prey-consumption and preference in Tsavo, Kenya. A lion-specific biomass model applied to prey frequencies in scats revealed that more than 85% of lion diet consisted of large ungulates weighing over 150 kg. While large ungulates were also preferred prey items in terms of their availability, we found a disproportionately high consumption and preference of lions for the endangered hirola and Grevys zebra-- species that were introduced in Tsavo as part of ex-situ conservation programs. Hirola and Grevys zebra populations have historically remained small in Tsavo despite strong recovery efforts, and our results likely indicate a disproportionate impact of lion predation on these small but crucial populations. Preferential predation, coupled with high availability of alternative prey, may trap hirola and Grevys zebra within a predator-pit. Our findings have strong implications for understanding lion diet, optimal foraging, and the potential effects predators have on endangered prey species in a landscape of critical conservation importance.

ecology↗