Proline Excretion and Indirect Suppression in Escherichia coli and Salmonella typhimurium

Abstract

The last step in proline biosynthesis in Escherichia coli K-12, Salmonella typhimurium LT7, and a number of other enterobacterial isolates is regulated so that no proline is excreted, even if excess Δ 1 -pyrroline-5-carboxylate, the immediate precursor of proline, is added to a culture. In proline auxotrophs blocked at an early step in proline biosynthesis ( proA or proB ), reversion to prototrophy is often due to a mutation in the arginine pathway which diverts N -acetyl glutamate γ-semialdehyde to proline synthesis, thus bypassing the proA or proB block. In such double mutants ( proAB, argD ), the last step in proline synthesis appears to be unregulated, since proline is excreted. Feedback inhibition and repression of the arginine pathway overcomes indirect suppression (restoring the Pro − phenotype), but proline regulation is not restored; double mutants still excrete proline when fed Δ 1 -pyrroline-5-carboxylate exogeneously. A new class of proline analogue-resistant mutant, due to mutation at argD , is also described.