Abstract: The replication terminator protein Fob1 of S. cerevisiae specifically interacts with two tandem Ter sites (replication fork barriers or RFBs) located in the non-transcribed spacer of rDNA to cause polar fork arrest. The Fob1-Ter complex is multifunctional and controls other DNA transactions such as recombination, by multiple mechanisms. Here, we report on the regulatory roles of the checkpoint proteins on the initiation and progression of recombination at Fob1-Ter complexes. The checkpoint adapter proteins Tof1 and Csm3 either positively or negatively controlled recombination depending on whether it was provoked by polar fork arrest or by transcription, respectively. The absolute requirements for these proteins for inducing recombination at an active replication terminus most likely masked their negative modulatory role at a later step of the process. Other checkpoint proteins of the checkpoint adapter/ mediator class such as Mrc1 and Rad9 that channel signals from the sensor to the effecter kinase, tended to suppress recombination at Fob1-Ter complexes regardless of how it was initiated. We have also discovered that the checkpoint sensor kinase Mec1 and the effecter Rad53 were positive modulators of recombination initiated by transcription but had little effect on recombination at Ter. The work also showed that the two pathways were Rad52-dependent but Rad51-independent. Since Ter sites occur in the intergenic spacer of rDNA from yeast to man, the mechanism is likely to be of widespread occurrence.