The mechanism of the auxotrophy for sulfur-containing amino acids imposed upon Escherichia coli by superoxide.

Defects in both of the genes coding for the cytosolic superoxide dismutases (SODs) of Escherichia coli impose an oxygen-dependent nutritional requirement for cysteine. This is now seen to be a bradytrophy, rather than an absolute auxotrophy, since lack of Cys merely imposed a growth lag and escape from this growth lag did not involve genetic reversion. This Cys bradytrophy was not seen in the SOD-competent parental strain, and it was relieved by a cell-permeant mimic of SOD activity; hence, it was due to O2-.. It was also relieved by an osmolyte, such as sucrose; hence, it appears due to leakage from the cell of some component needed for Cys biosynthesis. Medium conditioned by the aerobic growth of the SOD-defective strain relieved the growth lag. Bioassays with Cys mutants suggested that the conditioned medium contained SO3-3 or its equivalent, and sulfite per se was able to eliminate the growth lag. However, some component of the conditioned medium reacted with added sulfite and interfered with attempts to assay for it colorimetrically. These results suggest that the cell envelope of the SOD-defective strain was weakened, directly or indirectly, by O2 and then leaked sulfite. This prevents cysteine biosynthesis until sulfite accumulates in the medium.