Search bioRxiv⌕ Search

bioRxiv · 10.1101/2025.05.12.653485

Advancing global DNA-referencing of bushmeat in African tropical forests: a tool for identifying trade hotspots and dynamics in western and central Africa

Abstract

The bushmeat trade in Africa is a largely unregulated activity that drives the unsustainable exploitation of wild terrestrial vertebrates--an issue often coined the bushmeat crisis. We build on a four-gene mitochondrial DNA-typing approach to develop an unprecedented reference database framework for effectively tracing the bushmeat trade in tropical Africa. Our dataset comprises over 2,500 samples collected over a 13-yr period across 10 African countries and two European airports. Relying on an expert analytical pipeline and [~]8,700 nucleotide sequences, we identified 96% of samples to the species-level. In contrast, we estimated that conventional two-gene approaches would have yielded 18-26% erroneous or inconclusive taxonomic assignments. DNA-typing refined > 50% of field identifications, with refinement reaching 92-95% for highly processed carcasses seized in Europe. Leveraging expanded taxonomic representation, we empirically refined the genetic species thresholds applied to bushmeat and provide a reproducible pipeline for using our expert reference database from NCBI. Overall, we identified 133 species--mostly mammals--with one-third listed as of conservation concern, and uncovered cryptic diversity evidence within several taxa. Our results also demonstrated the value of community ecology indexes for large-scale monitoring of the bushmeat trade. While national markets generally mirrored regional biodiversity patterns across tropical Africa, Benin emerged as a notable outlier and a key wildlife trade hotspot. We advocate for the integration of community ecology frameworks into surveillance efforts to guide more effective, regionally tailored mitigation strategies. Continued, standardized sampling is essential to broaden taxonomic coverage and enhance detection of cryptic biodiversity in genetic bushmeat monitoring.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Pires, D., Gomes, C., Groom, B., Dufour, S., Danquah, E., Van Vliet, N., Ayecaba, G. N., Missoup, A. D., Afiademanyo, K., Djagoun, C. S., Gonedele, S. B., Chaber, A.-L., Olayemi, A., Antunes, A., Gaubert, P.. 2025-05-15. Advancing global DNA-referencing of bushmeat in African tropical forests: a tool for identifying trade hotspots and dynamics in western and central Africa. https://doi.org/10.1101/2025.05.12.653485

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Large language model-based bibliometric evaluation of population descriptors in human genetics

As the use of population descriptors such as race, ethnicity, and ancestry have become increasingly common in modern genetics research, there have been growing calls to critically examine their use. Most notably, in 2023, the National Academies of Science, Engineering, and Medicine (NASEM) published a report titled Using Population Descriptors in Genetics and Genomics Research: A New Framework for an Evolving Field, which included eight specific and actionable recommendations for researchers to implement the ethical and accurate use of population descriptors in genetic research. Here, we use the 2023 NASEM report as a benchmark to analyze the use of population descriptors in genome-wide association studies (GWAS). We develop a general toolkit for large language model-based bibliometrics, operationalize the report's recommendations into an evaluation framework, and apply this framework to evaluate all 4,007 papers from the GWAS Catalog published between 2007 and 2025 with full text available on PubMedCentral. We find significant improvements in adherence to NASEM report recommendations over time. However, most improvements predate the publication of the NASEM report itself, suggesting the report functioned primarily as a synthesis of existing best practices rather than a catalyst for change. We conclude by highlighting opportunities for growth in the field of human genetics.

genetics↗

Mitigating biases of rescaling in forward-in-time population genetic simulations

Forward-in-time population genetic simulations are widely used in evolutionary analyses, but simulating large populations and long genomic regions remains computationally demanding. To reduce this cost, parameter rescaling is widely employed, in which the original evolutionary process is approximated by one with a smaller population size and fewer generations. Recently, several studies using the SLiM simulator have raised concerns about the accuracy of this rescaling approach. In this study, we show that many of the biases reported in these studies can be mitigated by using a different simulation algorithm. These results reveal that the accuracy of parameter rescaling depends on how well the simulation algorithm preserves diffusion-limit properties under rescaling.

genetics↗

OPA1 controls mitochondrial dysfunction-driven liver fibrosis in MASLD

Progressive hepatic fibrosis is the principal determinant of morbidity and mortality in metabolic dysfunction-associated steatotic liver disease and steatohepatitis (MASLD/MASH). Mitochondrial dysfunction is a hallmark of MASH, and the release of mitochondrial damage-associated molecular patterns (mito-DAMPs) from injured hepatocytes can promote fibrosis. However, how mitochondrial dynamics and quality control shape the fibrotic response in MASLD/MASH remains unclear. Here, through large-scale genomic analyses of mitochondrial genes governing mitophagy, fusion and fission in human MASLD, with a power-equivalent sample size of approximately 700,000 individuals, we identify a strong association between hepatic fibrosis and the mitochondrial fusion factor dynamin-like GTPase optic atrophy 1 (OPA1). OPA1 transcripts and protein abundance in the liver epithelium were progressively dysregulated with advancing fibrosis. In mice, hepatocyte-specific OPA1 loss alone was sufficient to induce hepatic stellate cell activation and fibrosis in zone 3, promoted the release of mito-DAMPs into the circulation and exacerbated fibrosis in experimental MASH. These findings identify OPA1 as a central regulator of the hepatic fibrotic response and connect defective mitochondrial homeostasis to mito-DAMP release, hepatic stellate cell activation and fibrosis in MASLD.

genetics↗