Genomic rearrangements give rise to a range of genetic diseases, including cancer. Translin was isolated as a DNA binding protein, which was found to associate with translocation breakpoint junctions in many human tumours. However the cellular function of Transl in and its role in cancer progression is unknown. Translin has an interacting partner, TRAX (Translin-associated factor X). Translin and TRAX have been implicated in mRNA regulation, telomere stability, cell division, DNA repair and ribonuclease activity. Translin and TRAX are highly conserved and found in most eukaryotes, this suggests they may have a crucial function. We used the facile model system, Schizosaccharomyces pombe, to study the function of both TRAX and Translin. Results show that Translin and TRAX are not essential for growth, as deficient cells are viable. We found normal rates of mitotic proliferation and nonnal levels of intergenic and intragenic recombination, and we can also eliminate a key function in recovery from some types of DNA damage, but have identified a possible redundant role in the recovery from DNA damage. Genome rearrangements can be caused by replication fork barriers (RFBs). These can occur by transcription by RNA polymerase II (RNA pol II) resulting in recombination, known as transcription-associated recombination (TAR). However it is not known if RNA pol III-induced DNA replication fork stalling leads to an increase in recombination which might generate deleterious genetic changes. A single tRNAG1" gene placed in an ectopic locus can act as an RFP, and becomes a mitotic hotspot upon the loss of Swi I function. We have also identified an element of SB-boxes which creates a strong orientation-dependent RFB with no associated recombination.