Search bioRxiv⌕ Search

bioRxiv · 10.1101/2025.03.24.644985

Long-term hunter-gatherer continuity in the Rhine-Meuse region was disrupted by local formation of expansive Bell Beaker groups

Abstract

The first phase of the ancient DNA revolution painted a broad-brush picture of European Holocene prehistory, whereby 6500-4000 BCE, farmers descending from western Anatolians mixed with local hunter-gatherers resulting in 70-100% ancestry turnover, then 3000-2500 BCE people associated with the Corded Ware complex spread steppe ancestry into north-central Europe. We document an exception to this pattern in the wider Rhine-Meuse area in communities in the wetlands, riverine areas, and coastal areas of the western and central Netherlands, Belgium and western Germany, where we assembled genome-wide data for 109 people 8500-1700 BCE. Here, a distinctive population with high hunter-gatherer ancestry ([~]50%) persisted up to three thousand years later than in continental European regions, reflecting limited incorporation of females of Early European Farmer ancestry into local communities. In the western Netherlands, the arrival of the Corded Ware complex was also exceptional: lowland individuals from settlements adopting Corded Ware pottery had hardly any steppe ancestry, despite a characteristic early Corded Ware Y-chromosome. The limited influx may reflect the unique ecology of the regions river-dominated landscapes, which were not amenable to wholesale adoption of the early Neolithic type of farming introduced by Linearbandkeramik, making it possible for previously established groups to thrive, and creating a persistent but permeable boundary that allowed transfer of ideas and low-level gene flow. This changed with the formation-through-mixture of Bell Beaker using populations [~]2500 BCE by fusion of local Rhine-Meuse people (9-17%) and Corded Ware associated migrants of both sexes. Their expansion from the Rhine-Meuse region then had a disruptive impact across a much wider part of northwest Europe, including Britain where its arrival was the main source of a 90-100% replacement of local Neolithic peoples.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Olalde, I., Altena, E., Bourgeois, Q., Fokkens, H., Amkreutz, L., Deguilloux, M.-F., Fichera, A., Flas, D., Gandini, F., Kegler, J. F., Kootker, L. M., Leijnse, K., Kooijmans, L. L., Lauwerier, R., Miller, R., Molthof, H., Noiret, P., Raemaekers, D. C. M., Rivollat, M., Smits, L., Stewart, J. R., ten Anscher, T., Toussaint, M., Callan, K., Cheronet, O., Frost, T., Iliev, L., Mah, M., Micco, A., Oppenheimer, J., Patterson, I., Qiu, L., Soos, G., Workman, J. N., Edwards, C. J., Lazaridis, I., Mallick, S., Patterson, N., Rohland, N., Richards, M. B., Pinhasi, R., Haak, W., Pala, M., Reich, D.. 2025-03-25. Long-term hunter-gatherer continuity in the Rhine-Meuse region was disrupted by local formation of expansive Bell Beaker groups. https://doi.org/10.1101/2025.03.24.644985

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

KEEP EXPLORING

Related preprints

Genomic correlates of metastatic competence and progression in human melanoma

Genomic events and their timing that grant a primary tumour the competence to disseminate remain poorly defined. We performed sequencing of 247 stage I/II primary cutaneous melanomas (CMs) and 60 matched metastases without intervening therapy from a prospectively followed registry cohort with a median followup of 92 months, integrating copy-number, mutational, protein and spatial-transcriptomic analyses. Relapse was not distinguished by oncogenic point mutations, which were largely shared between primaries and metastases, but by somatic copy-number alterations (SCNAs) and global chromosomal instability. We defined OncoCycle, a six-gene copy-number signature (amplification of CDK4, MCL1 and CD276; biallelic loss of CDKN2A, CDKN2B and TP53BP1) that predicted relapse independently of established clinicopathological features in melanoma, and a pan-cancer analysis. In matched pairs, metastatic progression was driven by continued copy-number evolution and reduction in intra-tumoural heterogeneity, rather than by acquired point mutations, and OncoCycle alterations from primary tumours were preserved in metastasis seeding clones. Clonal reconstruction revealed both monoclonal and polyclonal metastasis seeding, and spatial transcriptomics resolved copy-number-defined metastatic subclones occupying and programming distinct immune and stromal niches. Thus, metastatic competence was primed early by focal SCNAs on a background of chromosomal instability, elaborated by continued copy-number evolution during dissemination and spatio-temporal interactions with the tumour-microenvironment.

genomics↗

PfPHAST: Plasmodium falciparum Public Health Amplicon Sequencing Tool, a Streamlined Panel for Malaria Genomic Surveillance

Genomic tools can support malaria control policy through surveillance of Plasmodium falciparum populations, tracking antimalarial drug resistance, pfhrp2/3 deletions that compromise rapid diagnostic tests, and selection at the circumsporozoite protein (PfCSP) vaccine target, as well as through molecular correction of therapeutic efficacy studies (TES). Multiplex Amplicons for Drug, Diagnostic, Diversity, and Differentiation Haplotypes using Targeted Resequencing (MAD4HatTeR), a comprehensive amplicon sequencing panel covering up to 276 targets, supports these applications but is tailored to research rather than routine programmatic use. We developed P. falciparum Public Health Amplicon Sequencing Tool (PfPHAST), a 56-target derivative of MAD4HatTeR spanning drug resistance loci, pfhrp2/3 deletion, PfCSP genotyping, non-falciparum species identification, and 20 high-heterozygosity microhaplotype loci for TES classification. We compared PfPHAST and MAD4HatTeR using laboratory strain controls, including two-strain dilution series and a five-strain mixture, across parasite densities of 100 to 10,000 parasites/L. At matched per-target depth, PfPHAST achieved a higher quality-control pass rate than MAD4HatTeR (94.4% versus 90.0%) and distributed reads more evenly across targets. The panels showed comparable recall and precision for drug resistance codons and microhaplotypes, reaching near-complete recall above 40% within-sample allele frequency (WSAF) at all densities, with reduced sensitivity for minor alleles below 10% WSAF at low parasite density in both panels. Observed and expected WSAF correlated strongly for both panels, and both resolved a five-strain polyclonal mixture, including a 5% minor strain. By concentrating sequencing capacity on targets of greatest programmatic relevance, PfPHAST offers a scalable, lower-cost alternative to comprehensive research panels without sacrificing performance on shared targets, complementing MAD4HatTeR for routine molecular malaria surveillance.

genomics↗

Structural variation in repeat elements is widespread in normal human tissues and in tumorigenesis

Somatic mosaicism contributes to genomic variation, yet postzygotic structural variants remain under-characterized. We performed long- and short-read WGS from multiple individuals (n=47 normal tissues; n=168 samples) and identified mosaic structural variants in all individuals and germ layers, impacting a median 285.2 kb/genome. Nearly half of breakpoints were independently validated, with tissue distributions reflecting both early and late developmental origins. Most mosaic variants were repeat-mediated and 8.3% overlapped functional elements, an enrichment compared to germline variants. To extend these analyses in samples where long-read sequencing is infeasible, we measured repeat alterations from short-read sequencing, recapitulating mosaic tissue-specific differences. We characterized tumor- and tissue- specific variation in repeats across 15 cancer types and found tumor-related repeat variation to be similar in scale to that of normal mosaic variation. Tracking repeat changes in cell-free DNA provided a noninvasive approach for tumor monitoring. Our analyses revealed widespread repeat-driven structural variation in health and disease.

genomics↗