Department of Biochemistry , University of Illinois at Urbana-Champaign , Roger Adams Laboratory, 600 S. Mathews Ave. , Urbana , Illinois 61801 , United States.
Carl R. Woese Institute for Genomic Biology , University of Illinois at Urbana-Champaign , 1206 W. Gregory Drive , Urbana , Illinois 61801 , United States.
ACS Chem Biol. 2019 Apr 19;14(4):742-750. doi: 10.1021/acschembio.9b00030. Epub 2019 Mar 13.
Rhizocticins are phosphono-oligopeptide antibiotics that contain a toxic C-terminal ( Z) -l -2-amino-5-phosphono-3-pentenoic acid (APPA) moiety. APPA is an irreversible inhibitor of threonine synthase (ThrC), a pyridoxal 5'-phosphate (PLP)-dependent enzyme that catalyzes the conversion of O-phospho-l-homoserine to l-threonine. ThrCs are essential for the viability of bacteria, plants, and fungi and are a target for antibiotic development, as de novo threonine biosynthetic pathway is not found in humans. Given the ability of APPA to interfere in threonine metabolism, it is unclear how the producing strain B. subtilis ATCC 6633 circumvents APPA toxicity. Notably, in addition to the housekeeping APPA-sensitive ThrC ( BsThrC), B. subtilis encodes a second threonine synthase (RhiB) encoded within the rhizocticin biosynthetic gene cluster. Kinetic and spectroscopic analyses show that PLP-dependent RhiB is an authentic threonine synthase, converting O-phospho-l-homoserine to threonine with a catalytic efficiency comparable to BsThrC. To understand the structural basis of inhibition, we determined the crystal structure of APPA bound to the housekeeping BsThrC, revealing a covalent complex between the inhibitor and PLP. Structure-based sequence analyses reveal structural determinants within the RhiB active site that contribute to rendering this ThrC homologue resistant to APPA. Together, this work establishes the self-resistance mechanism utilized by B. subtilis ATCC 6633 against APPA exemplifying one of many ways by which bacteria can overcome phosphonate toxicity.
类脂肽是含有有毒 C 末端(Z)-l-2-氨基-5-膦酸-3-戊烯酸(APPA)部分的磷酸化寡肽抗生素。APPA 是苏氨酸合酶(ThrC)的不可逆抑制剂,ThrC 是一种依赖吡哆醛 5'-磷酸(PLP)的酶,催化 O-磷酸-l-高丝氨酸转化为 l-苏氨酸。ThrC 对于细菌、植物和真菌的生存至关重要,是抗生素开发的靶点,因为从头合成途径的 l-苏氨酸生物合成途径在人类中不存在。鉴于 APPA 干扰苏氨酸代谢的能力,尚不清楚产生菌株枯草芽孢杆菌 ATCC 6633 如何规避 APPA 毒性。值得注意的是,枯草芽孢杆菌除了含有管家 APPA 敏感 ThrC(BsThrC)外,还编码第二个苏氨酸合酶(RhiB),该酶位于类脂肽生物合成基因簇内。动力学和光谱分析表明,PLP 依赖性 RhiB 是一种真正的苏氨酸合酶,可将 O-磷酸-l-高丝氨酸转化为苏氨酸,催化效率可与 BsThrC 相媲美。为了了解抑制的结构基础,我们确定了与管家 BsThrC 结合的 APPA 的晶体结构,揭示了抑制剂与 PLP 之间的共价复合物。基于结构的序列分析揭示了 RhiB 活性位点内的结构决定因素,这些因素有助于使这种 ThrC 同源物对 APPA 具有抗性。总之,这项工作确立了枯草芽孢杆菌 ATCC 6633 对抗 APPA 所利用的自我抵抗机制,这是细菌克服膦酸毒性的众多方式之一。