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Description
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Meiotic recombination ensures accurate chromosome segregation and promotes genetic diversity by generating crossovers between homologous chromosomes. While essential in most sexually reproducing organisms, recombination is variably regulated and can be absent in some lineages, a condition known as achiasmy. However, obligate achiasmy in both sexes of an otherwise sexual species has not been previously documented. Here, we investigate the beak-sedge Rhynchospora tenuis, a holocentric plant with the lowest known chromosome number among flowering plants (n = 2) and inverted meiosis. Using chromosome-scale genome assemblies from nine accessions, molecular cytogenetics, immunocytochemistry, high-throughput single-gamete sequencing and whole-genome sequencing of controlled crosses, we show that R. tenuis undergoes obligate, genome-wide achiasmy in both male and female meiosis. Despite normal early meiotic axis formation, synapsis fails, crossovers are not detected cytologically or genetically, and univalents persist at metaphase I. Extensive haplotype-specific accumulation of transposable elements (TEs) and reciprocal translocations drive strong segregation distortion, favouring the transmission of larger, TE-rich chromosomes. Remarkably, sexual reproduction is retained with fertilisation producing viable seeds only when translocation-compatible gametes meet, indicating strong post-meiotic selection in eliminating incompatible homozygous combinations. As a result, all surviving offspring are heterozygous and genetically identical to the maternal genotype, effectively restoring heterozygosity each generation and mimicking clonal reproduction. We propose that the combined effects of recombination loss, low chromosome number, holocentricity, inverted meiosis, and selective transmission of longer chromosomes enable faithful segregation and clonal-like inheritance despite sexual reproduction. These findings challenge the boundary between sex and clonality and reveal a unique evolutionary strategy linking genome architecture, recombination loss, and transmission bias.
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