MRN –CtIP protein complexes in humans have been implicated in the resistance of cancer cells tocamptothecin(CPT). The experiment investigated randomly mutated ctp1 gene, in S. pombe, which is a homolog of CtIP, to discover mutations on ctp1DNA sequencethat lead to sensitivity to CPT but not to other genotoxins. Cre -lox RMCE was performedin vitroto recombine cassettes carrying mctp1into cre expression plasmidpAW8 -ccdb, and transformed into E. colito generate a plasmid library. Plasmid library weretransformed into S. pombeand cre expression on plasmid switched on to catalyze in situRMCE,whichrecombined mctp1 into endogenous gene location in S. pombebase strain, in place of ura4+marker. In order to create library of mutants for screening colonies that showed sensitivity to drug agents, ura4-cells possessing mctp1 cells were selected for by the action of 5FOA and propagated to screen CPT (4μM&8μM), MMS (0.004% & 0.008%) and phleomycin (2.5μg/ml&3.5μg/ml). A total of eight plate-isolates sensitive to one or more genotoxins were discovered,of which one isolate showed sensitivity to CPT alone. This reiterated that defects in ctp1 results insensitivity to genotoxins, due to inability of defective mctp1to activate Mre11complex andbring about DSB resection and repair. However, screening for isolates isa statistical effort that requires continuous building up of libraries to generate more data that could provide more outcomes.Therebyunderlying molecular effects of unique isolate that showed phenotype to CPT could not be analyzed to draw more conclusions.