bioRxiv Science⌕ Search

bioRxiv · 10.1101/2025.07.10.664216

Chromosome Size as a Universal Predictor of Recombination Rate: Insights from Holocentric and Monocentric Systems

Abstract

Recombination is a fundamental evolutionary process essential for generating genetic diversity, facilitating adaptation, and driving speciation. However, direct measurement of recombination rate remains challenging, as standard methods--such as chiasma counts or genetic linkage maps--are labor-intensive and often infeasible for non-model species. In this study, we identify chromosome number and mean chromosome size as practical proxies for genome-wide recombination rate by analyzing genetic map data from 73 insect species and supplementary analyses of 157 monocentric flowering plants. We confirm the long-standing hypothesis that monocentric species have nearly twice as many crossovers per chromosome as holocentric species, reflecting structural constraints imposed by diffuse centromeres. Using both ordinary and phylogenetically informed Bayesian regression models, we show that recombination rate increases with chromosome number and decreases with mean chromosome size. Crucially, mean chromosome size is a significantly better predictor, particularly in holocentric species. This insight enables recombination rate estimation in thousands of species with known genome and chromosome sizes, thereby allowing hypothesis testing at scales previously unattainable. Building on these results, we present predictive models applicable to poorly studied holocentric plants. Overall, our study highlights the pivotal role of chromosome architecture in recombination evolution and provides an accessible framework for evolutionary genomic research across diverse lineages. Article summaryWhy do some species have more genetic shuffling than others? We investigated 73 insect species with detailed genetic maps and found that mean chromosome size is the best predictor of genome-wide recombination rate, not the number of chromosomes. This means we can now estimate recombination rates even in species where genetic maps are unavailable, using only genome size and chromosome number. We also show that chromosome structure matters--species with a single centromere per chromosome (monocentric) have nearly double the recombination compared to those with diffuse centromeres (holocentric). These insights open new doors for studying evolution across many organisms.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Zedek, F., Bures, P., Elliott, T. L., Escudero, M., Lucek, K., Marques, A.. 2025-07-16. Chromosome Size as a Universal Predictor of Recombination Rate: Insights from Holocentric and Monocentric Systems. https://doi.org/10.1101/2025.07.10.664216

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↗