结核分枝杆菌β-酮酰基-酰基载体蛋白合酶III的活性通过单个苏氨酸残基的磷酸化作用而受到抑制。
The Mycobacterium tuberculosis beta-ketoacyl-acyl carrier protein synthase III activity is inhibited by phosphorylation on a single threonine residue.
作者信息
Veyron-Churlet Romain, Molle Virginie, Taylor Rebecca C, Brown Alistair K, Besra Gurdyal S, Zanella-Cléon Isabelle, Fütterer Klaus, Kremer Laurent
机构信息
Laboratoire de Dynamique des Interactions Membranaires Normales et Pathologiques, Universités de Montpellier II et I, CNRS UMR 5235, INSERM, Place Eugène Bataillon, 34095 Montpellier Cedex 05, France.
出版信息
J Biol Chem. 2009 Mar 6;284(10):6414-24. doi: 10.1074/jbc.M806537200. Epub 2008 Dec 11.
Mycolic acids are hallmark features of the Mycobacterium tuberculosis cell wall. They are synthesized by the condensation of two fatty acids, a C56-64-meromycolyl chain and a C24-26-fatty acyl chain. Meromycolates are produced via the combination of type I and type II fatty acid synthases (FAS-I and FAS-II). The beta-ketoacyl-acyl carrier protein (ACP) synthase III (mtFabH) links FAS-I and FAS-II, catalyzing the condensation of FAS-I-derived acyl-CoAs with malonyl-ACP. Because mtFabH represents a potential regulatory key point of the mycolic acid pathway, we investigated the hypothesis that phosphorylation of mtFabH controls its activity. Phosphorylation of proteins by Ser/Thr protein kinases (STPKs) has recently emerged as a major physiological mechanism of regulation in prokaryotes. We demonstrate here that mtFabH was efficiently phosphorylated in vitro by several mycobacterial STPKs, particularly by PknF and PknA, as well as in vivo in mycobacteria. Analysis of the phosphoamino acid content indicated that mtFabH was phosphorylated exclusively on threonine residues. Mass spectrometry analyses using liquid chromatography-electrospray ionization/tandem mass spectrometry identified Thr45 as the unique phosphoacceptor. This was further supported by complete loss of PknF- or PknA-dependent phosphorylation of a mtFabH mutant. Mapping Thr45 on the crystal structure of mtFabH illustrates that this residue is located at the entrance of the substrate channel, suggesting that the phosphate group may alter accessibility of the substrate and thus affect mtFabH enzymatic activity. A T45D mutant of mtFabH, designed to mimic constitutive phosphorylation, exhibited markedly decreased transacylation, malonyl-AcpM decarboxylation, and condensing activities compared with the wild-type protein or the T45A mutant. Together, these findings not only represent the first demonstration of phosphorylation of a beta-ketoacyl-ACP synthase III enzyme but also indicate that phosphorylation of mtFabH inhibits its enzymatic activity, which may have important consequences in regulating mycolic acid biosynthesis.
分枝菌酸是结核分枝杆菌细胞壁的标志性特征。它们由两种脂肪酸缩合而成,一种是C56 - 64的分枝菌酸链和一种C24 - 26的脂肪酰基链。分枝菌酸通过I型和II型脂肪酸合酶(FAS-I和FAS-II)的组合产生。β-酮酰基-酰基载体蛋白(ACP)合酶III(mtFabH)连接FAS-I和FAS-II,催化FAS-I衍生的酰基辅酶A与丙二酰-ACP的缩合反应。由于mtFabH代表分枝菌酸途径的一个潜在调控关键点,我们研究了mtFabH的磷酸化控制其活性的假说。丝氨酸/苏氨酸蛋白激酶(STPKs)对蛋白质的磷酸化最近已成为原核生物中一种主要的生理调控机制。我们在此证明,mtFabH在体外能被几种分枝杆菌的STPKs有效磷酸化,特别是被PknF和PknA磷酸化,在分枝杆菌体内也能被磷酸化。对磷酸氨基酸含量的分析表明,mtFabH仅在苏氨酸残基上被磷酸化。使用液相色谱 - 电喷雾电离/串联质谱的质谱分析确定Thr45是唯一的磷酸化位点。mtFabH突变体的PknF或PknA依赖性磷酸化完全丧失进一步支持了这一点。将Thr45定位在mtFabH的晶体结构上表明,该残基位于底物通道的入口处,这表明磷酸基团可能会改变底物的可及性,从而影响mtFabH的酶活性。设计用于模拟组成型磷酸化的mtFabH的T45D突变体,与野生型蛋白或T45A突变体相比,其转酰基化、丙二酰 - AcpM脱羧和缩合活性明显降低。总之,这些发现不仅首次证明了β-酮酰基-ACP合酶III的磷酸化,还表明mtFabH的磷酸化抑制其酶活性,这可能对调控分枝菌酸生物合成具有重要意义。