Fig. 6

Transcription-replication conflict-induced R-loops correlated with meiotic DSB formation. (A) The signal intensity profiles of R-loop peaks (0 h, 0.5 h, 2 h, Pac) in regions ± 1 kb from the centre of codirectional collisions (the orientation of gene transcription and DNA replication in the same direction) and head-on collisions (the orientation of gene transcription and DNA replication in the opposite direction) identified with the orientation of gene transcription and the localization of ARS regions, respectively. The annotations of the codirectional collision regions and head-on collision regions are shown in (A). (B) Metaplots of wR-loop peaks centred on codirectional collisions and head-on collisions identified with the orientation of gene transcription and the localization of ARS regions. (C) Metaplots of cR-loop peaks centred on codirectional collisions and head-on collisions identified with the orientation of gene transcription and the localization of ARS regions. (D) A representative genomic region covering the ARS309 and ADY2 head-on collision region (chrIII:130,736 − 133,314), showing R-loop signals (0 h, 0.5 h, 2 h, Pac) sharing overlap with meiotic DSBs [7]. (E) Venn plots showing the overlays of Spo11-oligo-seq peaks [7] and head-on collision regions. (F) Permutation test of colocalization between Spo11-oligo-seq peaks and head-on collision regions. Evobs, evaluation observe; Evperm, evaluation permutation. (G) The signal intensity profiles of cR-loop peaks in regions ± 0.5 kb from the centre of head-on collisions in the WT and spo11Δ strains at 2 h after sporulation. cR-loop signal intensities were calculated and normalized by subtracting basal levels of signal intensities. (H) A representative genomic region covering the ARS3315 and TAH1 head-on collision region, ARS1415 and BNI5 head-on collision region in the WT and spo11Δ strains at 2 h after sporulation, showing R-loop signals sharing overlap with meiotic DSBs.