Fig. 1: Polymerase theta-independent repair of G-quadruplex-induced DSBs is driven by flanking sequence homology.

a Model explaining DSB formation and repair at replication-blocking G-quadruplex structures³¹. b Size distribution of deletions that accumulate in the genomes of dog-1 and dog-1 polq-1 mutant animals (dog-1 data from³²). c Potential mechanism explaining the formation of the deletions marked in b. d Schematic diagram of four endogenous G4 loci with different degrees of flanking homology. The most prominent repeated sequences are indicated in blue. e Representative images of PCR-based analysis of the indicated G4-containing loci. Each lane contains the genomic DNA of three adult animals. Asterisks indicate stochastic deletions, which manifest as shorter than wild-type products and Δ indicates the size range of the PCR-amplified deletion products. Deletion sequences are provided as a Source Data file. f Graphic illustration of G4 deletions profiles at four endogenous G4 loci. For each locus typical G4 deletions in dog-1 and dog-1 polq-1 animals are depicted. Black bars represent homology-independent deletions; red bars represent homology-dependent events. g Histogram depicting relative deletion frequencies at the indicated G4 loci as determined by the presence of deletion bands in the PCR-based assay on single worms of dog-1 (grey bars) and dog-1 polq-1 mutant animals (black bars). Depicted frequencies are relative to the deletion frequency in dog-1 single mutants to allow the comparison of loci expressing different stochastic G4 deletion rates. The number of analysed animals is depicted on top of the bars. Gel counts are provided as a Source Data file.