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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. 

Abstract Genomic clusters of immune genes, including those encoding nucleotide-binding leucine-rich repeat (NLR) proteins, are a model for exploring the dynamics of genomic regions in flux. Rapid sequence evolution of immune genes, including NLRs, and variation in their gene content, may enable long-lived plants, which lack adaptive immune systems, to keep pace with the fast evolution of pathogens. To explore the patterns and processes shaping the evolution of NLR gene content in a genus of long-lived tree species, we unified the annotation of NLR genes across 11 accessions (or 15 haplotypes) from the genusCitrusand its relatives, including three new diploid genome assemblies. A majority of NLRs were arranged in genomic clusters composed of paralogous genes, typically from a single gene family. Even larger clusters, with 10 or more NLRs, were limited to genes derived from one or few gene families. These patterns suggested that genomic clustering of NLRs arose through local expansion of phylogenetically related NLRs, but the mechanistic processes driving these patterns are not clear. Local gene duplication can be mediated by multiple processes, including transposon-mediated gene capture and subsequent proliferation, and non-allelic repair of double stranded breaks, including unequal recombination. Examples of retrotransposon-mediated duplication of NLRs were identified, but these were not sufficient to explain massive regional expansions. Signatures of unequal recombination are challenging to identify. Focusing on recent lineage-specific sequence duplications, at least one case of unequal recombination was identified, supporting a role for unequal recombination in shaping genomic variation in these regions. 

Abstract Aluminum‐dependent stoppage of root growth requires the DNA damage response (DDR) pathway including the p53‐like transcription factor SUPPRESSOR OF GAMMA RADIATION 1 (SOG1), which promotes terminal differentiation of the root tip in response to Al dependent cell death. Transcriptomic analyses identified Al‐induced SOG1‐regulated targets as candidate mediators of this growth arrest. Analysis of these factors either as loss‐of‐function mutants or by overexpression in theals3‐1background shows ERF115, which is a key transcription factor that in other scenarios is rate‐limiting for damaged stem cell replenishment, instead participates in transition from an actively growing root to one that has terminally differentiated in response to Al toxicity. This is supported by a loss‐of‐functionerf115mutant raising the threshold of Al required to promote terminal differentiation of Al hypersensitiveals3‐1. Consistent with its key role in stoppage of root growth, a putativeERF115barley ortholog is also upregulated following Al exposure, suggesting a conserved role for this ATR‐dependent pathway in Al response. In contrast to other DNA damage agents, these results show that ERF115 and likely related family members are important determinants of terminal differentiation of the root tip following Al exposure and central outputs of the SOG1‐mediated pathway in Al response.