The mutant bacteriophage Mu gem2(Ts), known to synchronize the division of infected cells, to relax DNA supercoiling and, as prophage, to give rise to precisely excised revertants, has been thought to overexpress the gemA-mor operon, and genetic evidence suggests that the B subunit of DNA gyrase (GyrB) is the target of action of GemA. In two different double hybrid tests presented here, we find no evidence of GemA-GyrB protein-protein interaction. We do observe a GemA-GemA interaction, however, indicating that GemA can dimerize. In lacZ::Mu lysogens, overexpression of the gemA-mor operon from a plasmid, under control of the L-arabinose inducible p araBAD promoter, does not permit the recovery of Lac + revertants. These observations suggest that GyrB is not the direct target of GemA action and that the various phenotypes of Mu gem2(Ts) are not caused by overexpression of the gemA-mor operon.