Val D L, Cronan J E
Department of Microbiology, University of Illinois, Urbana, Illinois 61801, USA.
J Bacteriol. 1998 May;180(10):2644-51. doi: 10.1128/JB.180.10.2644-2651.1998.
Many gram-negative bacteria synthesize N-acyl homoserine lactone autoinducer molecules as quorum-sensing signals which act as cell density-dependent regulators of gene expression. We have investigated the in vivo source of the acyl chain and homoserine lactone components of the autoinducer synthesized by the LuxI homolog, TraI. In Escherichia coli, synthesis of N-(3-oxooctanoyl)homoserine lactone by TraI was unaffected in a fadD mutant blocked in beta-oxidative fatty acid degradation. Also, conditions known to induce the fad regulon did not increase autoinducer synthesis. In contrast, cerulenin and diazoborine, specific inhibitors of fatty acid synthesis, both blocked autoinducer synthesis even in a strain dependent on beta-oxidative fatty acid degradation for growth. These data provide the first in vivo evidence that the acyl chains in autoinducers synthesized by LuxI-family synthases are derived from acyl-acyl carrier protein substrates rather than acyl coenzyme A substrates. Also, we show that decreased levels of intracellular S-adenosylmethionine caused by expression of bacteriophage T3 S-adenosylmethionine hydrolase result in a marked reduction in autoinducer synthesis, thus providing direct in vivo evidence that the homoserine lactone ring of LuxI-family autoinducers is derived from S-adenosylmethionine.
许多革兰氏阴性菌合成N-酰基高丝氨酸内酯自诱导分子作为群体感应信号，这些信号作为基因表达的细胞密度依赖性调节因子。我们研究了由LuxI同源物TraI合成的自诱导物的酰基链和高丝氨酸内酯成分的体内来源。在大肠杆菌中，TraI合成N-(3-氧代辛酰基)高丝氨酸内酯在β-氧化脂肪酸降解受阻的fadD突变体中不受影响。此外，已知诱导fad操纵子 的条件并未增加自诱导物的合成。相反，脂肪酸合成的特异性抑制剂头孢菌素和重氮硼烷即使在依赖β-氧化脂肪酸降解生长的菌株中也能阻断自诱导物的合成。这些数据提供了首个体内证据，表明由LuxI家族合成酶合成的自诱导物中的酰基链来源于酰基-酰基载体蛋白底物而非酰基辅酶A底物。此外，我们表明，噬菌体T3 S-腺苷甲硫氨酸水解酶的表达导致细胞内S-腺苷甲硫氨酸水平降低，从而使自诱导物合成显著减少，因此提供了直接的体内证据，表明LuxI家族自诱导物的高丝氨酸内酯环来源于S-腺苷甲硫氨酸。
