When E. coli WU3610 (tyrA14 ochre) bacteria are starved of tyrosine on the surface of glucose-salts agar plates, there is a progressive accumulation of slow growing prototrophic mutants that are neither revertants at the ochre codon nor any of the well characterised tRNA ochre suppressors. Isogenic derivatives defective in transcription repair coupling factor (mfd) showed normal starvation-associated mutation (SAM). WU361045, the original mfd strain, showed very much reduced SAM. At 37 degrees C this was associated with progressive loss of viability on plates but the defect in SAM was not due to loss of viability since incubation at 27 degrees C or addition of catalase prevented the loss of viability but did not restore SAM. Furthermore, mutants could not be rescued from starved WU361045 populations by a short period of tyrosine supplementation arguing that WU361045 was defective not in the survival of starvation-associated mutants, but in their formation. The SAM defect in WU361045 was not complemented by the katF gene on a low copy number plasmid. It is concluded that WU361045 carries an unidentified mutation, not under katF control, that greatly reduces SAM. If SAM is attributable to a spontaneously occurring DNA lesion, the latter is unlikely to be formed by hydrogen peroxide or active species derived from it.