Fig. 4: HELQ-1 acts in synthesis-dependent strand annealing and suppresses tandem duplications.

a Models for SSA and SDSA repair of DSBs. Homologous stretches of DNA are depicted in dark blue. b Schematic representation of the SDSA reporter³⁹. A DSB can be introduced by the I-SceI endonuclease at its recognition site positioned within a corrupted GFP expression cassette. SDSA repair using a GFP segment cloned downstream of the expression cassette will restore the GFP ORF leading to GFP expressing animals. c Histograms depicting the average number of GFP expressing cells per worm for the indicated genotype. Experiments are performed in triplicate (*P < 0.05, **P < 0.01; two-sided t-tests). P value WT vs. brc-1: 0.0085. P value WT vs. helq-1: 0.0115. Each dot represents the average number of each replicate. Error bars represent SEM. Quantifications are provided as a Source Data file. d Schematic representation of the CRISPR/Cas9-induced gene correction assay. CRISPR-induced DSB at the dpy-10 locus can be repaired via end-joining or using an injected single-stranded oligo as a template. The sequence of the oligo differs from the target locus at the centre (in green). Mutation sequences are provided as a Source Data file. e Histogram depicting the different categories of repair outcomes. Insertions are depicted in yellow, simple deletions in grey, deletions containing insertion in red, outcomes of repair using the oligo are depicted in blue. The difference in ratio between ssODN-guided repair and indels were tested using Chi-square test (***P < 0.001). f Size distribution of structural variations that accumulate in the genomes of the indicated genotype (wild-type data derived from ref. ⁴⁶). Mutation sequences are provided as a Source Data file. g Mechanistic model for the aetiology of tandem duplications (TDs) in helq-1 mutant genetic backgrounds.