(A) R-loops that cause DSBs persist at the break site. Early HR events (resection, homology search, strand capture and invasion) proceed as normal for one side of the break, but are inhibited by the presence of an R-loop on the opposite side. If RNase H1 or H2 act to clear the hybrid, repair can proceed as normal. If the hybrid persists, the second strand cannot be captured and the cell engages BIR. (B) BIR at the rDNA encounters replication blocks and slows. These replication blocks (over/under-winding, transcribing or stalled RNA polI, R-loops) are exacerbated in the absence of Top1, creating unresolvable structures that lead to cell death. PIF1 and POL32 mutants make BIR less processive, allowing BIR machinery to disengage before lethality occurs. The repair mechanism used after BIR is disengaged is unknown. RPA190 mutants allow for resolution of these structures, perhaps by disengaging RNA pol I through termination or backtracking activities.