Osmoprotectant-dependent expression of plcH, encoding the hemolytic phospholipase C, is subject to novel catabolite repression control in Pseudomonas aeruginosa PAO1.
Osmoprotectant-dependent expression of plcH, encoding the hemolytic phospholipase C, is subject to novel catabolite repression control in Pseudomonas aeruginosa PAO1.
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编码溶血磷脂酶 C 的 plcH 的渗透保护剂依赖性表达受到铜绿假单胞菌 PAO1 中新型分解代谢物抑制的控制。
DOI：
10.1128/jb.179.15.4874-4881.1997
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发表时间：
1997
影响因子：
3.2
通讯作者：
Vasil,ML
中科院分区：
文献类型：
--
作者：
Sage,AE;Vasil,ML
铜绿假单胞菌的溶血磷脂酶C（PlcH）的表达在磷酸盐饥饿条件下或在存在保护剂胆碱和甘氨酸甜菜碱的情况下被诱导。因为胆碱和甘氨酸甜菜碱除了赋予铜绿假单胞菌抗氧化保护作用之外还可以作为碳源和能源，所以似乎plcH的诱导可能受到三羧酸循环中间体如琥珀酸盐的分解代谢物阻遏控制（CRC）。补充有20 mM琥珀酸盐的铜绿假单胞菌PAO 1的经β-内酰胺保护剂诱导的培养物中的总磷脂酶（PLC）活性比补充有非分解代谢产物抑制底物乳酸盐的培养物中的水平低三至四倍。在含有plcH：：lacZ操纵子融合体的菌株PAO 1的衍生物中，对plcH依赖性plcH表达的分析表明：（i）琥珀酸盐阻止了plcH表达被plcH保护剂诱导;和（ii）琥珀酸盐的添加减少或关闭了plcH在plcH诱导的细菌中的进一步表达，而补充有乳酸盐的培养物在plcH表达中几乎没有变化或没有变化。RNA酶保护分析证实，抑制plcH发生在转录水平。然而，在CRC中解耦的铜绿假单胞菌突变体在plcH表达的琥珀酸依赖性抑制方面表现出与野生型菌株（PAO 1）相似的表型。渗透保护素诱导的总PLC活动，与相同的plcH：：lacZ融合测量的plcH的表达水平，和plcH的转录水平在CRC缺陷型菌株反映了在菌株PAO 1中看到的。这表明plcH的CRC通过与调节葡萄糖或甘露醇分解代谢途径不同的独特机制起作用。携带vfr突变的菌株（其编码铜绿假单胞菌中的大肠杆菌Crp同源物）仍表现出野生型表型，其具有plcH的胞内保护素依赖性表达和CRC。这些数据表明，有一种新的CRC系统，调节铜绿假单胞菌中plcH的表达。
Expression of the hemolytic phospholipase C (PlcH) of Pseudomonas aeruginosa is induced under phosphate starvation conditions or in the presence of the osmoprotectants choline and glycine betaine. Because choline and glycine betaine may serve as carbon and energy sources in addition to conferring osmoprotection to P. aeruginosa, it seemed possible that induction of plcH is subject to catabolite repression control (CRC) by tricarboxylic cycle intermediates such as succinate. Total phospholipase (PLC) activity in osmoprotectant-induced cultures of P. aeruginosa PAO1 supplemented with 20 mM succinate was three- to fourfold lower than the levels in cultures supplemented with the non-catabolite-repressive substrate lactate. Analyses of osmoprotectant-dependent plcH expression in a derivative of strain PAO1 containing a plcH::lacZ operon fusion showed that (i) succinate prevented induction of plcH expression by osmoprotectants; and (ii) addition of succinate reduced or shut down further expression of plcH in osmoprotectant-induced bacteria, while cultures supplemented with lactate had little or no change in plcH expression. RNase protection analysis confirmed that repression of plcH occurs at the transcriptional level. However, a P. aeruginosa mutant decoupled in CRC exhibited a phenotype similar to that of the wild-type strain (PAO1) with respect to succinate-dependent repression of plcH expression. Osmoprotectant-induced total PLC activities, levels of expression of plcH measured with the same plcH::lacZ fusion, and levels of plcH transcription in a CRC-deficient strain reflected those seen in strain PAO1. This indicates that CRC of plcH functions by a distinct mechanism which differs from that regulating the glucose or mannitol catabolic pathway. A strain carrying a mutation in vfr, which encodes the Escherichia coli Crp homolog in P. aeruginosa, still exhibited a wild-type phenotype with respect to osmoprotectant-dependent expression and CRC of plcH. These data indicate that there is a novel CRC system that regulates the expression of plcH in P. aeruginosa.