Body TRS mutants thus fell into two distinct types, determined by the position and chemistry of the substitution. In mutants of the ®rst type, sg RNA synthesis was impaired mainly because of the disruption of the leader± body TRS duplex. This effect could be compensated for by introduction of the corresponding mutation in the leader TRS and, in the double mutant, sg RNA synthesis was restored compared with the corresponding single mutants. In mutants of the second type, sg RNA synthesis was down-regulated as a consequence of both TRS duplex disruption and disruption of the primary sequence (or secondary structure) of the body TRS. Obviously, the latter effect could not be compensated for by mutating the leader TRS, and the corresponding double mutants did not show restoration of sg RNA synthesis.