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

Figure 7. Limited Availability of DNA Repair Proteins Explains the Requirement of Dmc1 for SSA at VDE-DSBs.

Figure 7

In wild-type meiosis there is sufficient resection complex and Rfa1 to create and bind to long tracts of ssDNA at the VDE-DSB so that SSA is possible. In part, the ready supply of such proteins is likely created by the asynchronous nature of Spo11-DSB formation and repair in the nucleus, thus when some Spo11-DSBs are using these proteins others may have moved to a biochemical step that allows their release. In dmc1Δ cells, so much resection complex and Rfa1 is sequestered to multiple unprepared Spo11-DSBs that insufficient resection complex is available to create long resection tracts at the VDE-DSB; or in cases where long resection tracts appear there is not enough free Rfa1 to bind the repeated sequences. Mutating either SPO11 or SAE2 relaxes the demand on both resection proteins and ssDNA binding proteins such that resection and repair of the VDE-DSB is no longer limiting.