Somatic selection shapes mutation accumulation in Citrus sinensis

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ID: 329118
2026
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Abstract
Abstract An organism becomes genetically mosaic through the accumulation of somatic mutations. Genetic mosaicism is a commonality of multicellular life and has been studied extensively in humans due to its associations with aging and diseases. In humans, somatic selection shapes the accumulation of somatic mutations, with strong signatures of positive somatic selection in cancer cell lineages. So far, evidence for somatic selection in plants has been inconsistent. The evolutionary implications of genetic mosaicism in humans and other animals are limited by early specification of germline cells, preventing transmission of somatic mutations to progeny. In contrast, many plant lineages reproduce asexually with clonal progeny derived from vegetative tissues. We describe the patterns and processes shaping somatic mutation accumulation within a single, 149-year-old historic sweet orange (Citrus sinensis) tree and within a clonal lineage of sweet orange. More than 12,000 somatic mutations were identified in the historic tree and 28,000 somatic mutations were identified across 199 clonally related sweet orange accessions. Both the spatial and genomic distributions of somatic mutations are non-random. The spatial patterns of somatic mutations across the historic tree depend on tree growth and development and their accumulation across the tree canopy recapitulates branching topology. Analysis of the genomic distribution of somatic mutations revealed that the subtelomeres, which are large arrays of ∼180 bp repeats, are mutation hotspots. Finally, there was genomic evidence that somatic selection shapes the accumulation of somatic mutations both within the historic tree and also during clonal propagation.
Reference Key
openalex_W7213560859 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Taylor R Beaulieu, Emmanuel Ávila de Dios, Danelle K. Seymour
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Journal The Plant cell
Year 2026
DOI
10.1093/plcell/koag288
URL
https://doi.org/10.1093/plcell/koag288
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