ArticleG3 (Bethesda, Md.)2026
Tissue-specific DNA repair strategies underlie apparent high transposon activity in the Caenorhabditis elegans soma.
Article in G3 (Bethesda, Md.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Transposons are parasitic nucleic acids that threaten genome integrity in all organisms. DNA transposons mobilize via a cut-and-paste mechanism, which leads to double-strand breaks (DSBs). In Caenorhabditis elegans, DNA transposons are mobile in the soma, where their excision rates are reportedly ≅1,000-fold higher than in germ cells. How or why DNA transposons might be highly active in the C. elegans soma is a mystery. Here, we show that the non-homologous end joining (NHEJ) pathway is responsible for generating >99.9% of the empty transposon sites accruing in the C. elegans soma. C. elegans uses homologous recombination (HR) to repair transposon-induced DSBs in its germline. Because HR, but not NHEJ, restores excised transposons back into their original chromosomal position during repair, we propose that the apparent elevated activity of DNA transposons in the C. elegans soma can, in large part, be explained by tissue-specific differences in DNA repair strategy.
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