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. 2007 Nov 30;3(11):e223. doi: 10.1371/journal.pgen.0030223

Figure 4. Meiotic Prophase Arrest Does Not Inhibit VDE-DSB1 Repair, but the Quantity and State of Spo11-DSBs Affects the Need for Dmc1.

Figure 4

In all cases spo11 refers to spo11-Y135F-HA3His6.

(A) DNA from 0 h to 8 h of meiotic culture was digested and displayed as described in Figure 2C.

(B) Cells do not require Ndt80 function to turnover the VDE-DSB in DMC1 cells, and dmc1Δ is epistatic to ndt80 for VDE-DSB1 repair. The repair defect imposed by loss of Dmc1 function is fully rescued by (C and D) removing all or most Spo11-DSB formation in either spo11 or hop1 mutant cells and by (E) inhibiting resection at Spo11-DSBs by mutating SAE2.

(F) The epistatic relationships between the various mutations and dmc1 are also displayed by quantification of Δproduct after 8 h of meiotic culture, expressed as a proportion of parental arg4-vde chromatids. Wild type and dmc1 are shown for comparison. Reducing the quantity of Spo11-DSBs to 50% of wild-type levels using a strain heterozygous for different SPO11 alleles leads to partial relief of Dmc1 dependence for VDE-DSB1 repair.