Frank Johannes
Trees are long-lived plants characterized by the development of highly branched shoot systems. Along these structures, somatic mutations arise and may become fixed in reproductive tissues such as flowers and fruits. Because mature trees produce tens of thousands of terminal branches, limiting the accumulation of somatic mutations is critical to avoid mutational meltdown and inbreeding depression. Although recent evidence suggests that long-lived plants have evolved mechanisms that slow the buildup of somatic variants with age, the developmental basis for this remains unclear. Here, we derive a theoretical model linking crown development with cell lineage sampling to show that branching architecture strongly influences the accumulation of unique somatic mutations, often to the same extent as modulating the mutation rate itself. We find that tree forms that promote developmental path-sharing among branches restrict the spread of distinct cell lineages, lowering the crown-wide mutation burden by orders of magnitude even when mutation rates and branch numbers are held constant. This buffering effect suggests that branching strategies may evolve not only to optimize growth and resource allocation, but also to limit the genomic variation generated during ontogeny.