Berg C M, Rossi J J
J Bacteriol. 1974 Jun;118(3):928-34. doi: 10.1128/jb.118.3.928-934.1974.
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 Delta(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 gamma-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 Delta(1)-pyrroline-5-carboxylate exogeneously. A new class of proline analogue-resistant mutant, due to mutation at argD, is also described.
大肠杆菌K-12、鼠伤寒沙门氏菌LT7及其他一些肠道细菌分离株中脯氨酸生物合成的最后一步受到调控,因此即便向培养物中添加过量的脯氨酸直接前体——Δ¹-吡咯啉-5-羧酸,也不会有脯氨酸分泌。在脯氨酸生物合成早期步骤(proA或proB)受阻的脯氨酸营养缺陷型中,回复为原养型通常是由于精氨酸途径发生突变,该突变将N-乙酰谷氨酸γ-半醛转向脯氨酸合成,从而绕过了proA或proB的阻断。在这类双突变体(proAB,argD)中,脯氨酸合成的最后一步似乎不受调控,因为脯氨酸会被分泌出来。精氨酸途径的反馈抑制和阻遏克服了间接抑制(恢复Pro⁻表型),但脯氨酸调控并未恢复;当向双突变体外源投喂Δ¹-吡咯啉-5-羧酸时,它们仍会分泌脯氨酸。还描述了一类由于argD突变产生的新型脯氨酸类似物抗性突变体。