The observation that leader TRS mutations could bè rescued' by introducing complementary mutations in the body TRS, but that many body TRS mutations could not bè rescued' by corresponding changes in the leader TRS, is clearly illustrated by the U 1 A mutants. Due to the restoration of TRS base pairing possibilities, the RNA7 synthesis of double mutant DU 1 A was signi®cantly increased compared with that of LU 1 A, but not above the level of BU 1 A. Thus, restoration of the leader±body duplex in DU 1 A exerted a clear effect on sg RNA7 production compared with LU 1 A, but had no effect on sg RNA synthesis compared with BU 1 A. This exempli®ed the dominant nature of a mutation in the primary sequence of a body TRS. In contrast, for instance, the BC 2 U mutation probably affected duplex formation only, because RNA7 synthesis was restored almost to wildtype levels in the DC 2 U double mutant.