SummaryWe demonstrate a role for Qri2 in the essential DNA repair function of the Smc5/6 complex inSaccharomyces cerevisiae. We generated temperature‐sensitive (ts) mutants inQRI2and characterized their properties. The mutants arrest after S phase and prior to mitosis. Furthermore, the arrest is dependant on the Rad24 checkpoint, and is also accompanied by phosphorylation of the Rad53 checkpoint effector kinase. The mutants also display genome instability and are sensitive to agents that damage DNA. Two‐hybrid screens reveal a physical interaction between Qri2 and proteins that arenon‐Smcelements of the Smc5/6 DNA repair complex, which is why we propose the nameNSE4for the open reading frame previously known asQRI2. A key role for Nse4 in Smc5/6 function is likely, as overexpressing known subunits of the Smc5/6 complex suppressesnse4tscell cycle arrest. Thense4tsgrowth arrest is non‐lethal and unlike the catastrophic nuclear fragmentation phenotype ofsmc6tsmutants, the nucleus remains intact; replicative intermediates and sheared DNA are not detected. This could imply a role for Nse4 in maintenance of higher order chromosome structure.