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首页> 外文期刊>Acta crystallographica. Section D, Structural biology. >Crystal structure of Mycobacterium tuberculosisFadB2 implicated in mycobacterial beta-oxidation
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Crystal structure of Mycobacterium tuberculosisFadB2 implicated in mycobacterial beta-oxidation

机译：分枝杆菌的晶体结构tuberculosisFadB2与分枝杆菌机会

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The intracellular pathogen Mycobacterium tuberculosis is the causative agent oftuberculosis, which is a leading cause of mortality worldwide. The survival ofM. tuberculosis in host macrophages through long-lasting periods of persistencedepends, in part, on breaking down host cell lipids as a carbon source. Thecritical role of fatty-acid catabolism in this organism is underscored by theextensive redundancy of the genes implicated in beta-oxidation (approx100 genes). In aprevious study, the enzymology of the M. tuberculosis L-3-hydroxyacyl-CoAdehydrogenase FadB2 was characterized. Here, the crystal structure of thisenzyme in a ligand-free form is reported at 2.1 A resolution. FadB2 crystallizedas a dimer with three unique dimer copies per asymmetric unit. The structure ofthe monomer reveals a dual Rossmann-fold motif in the N-terminal domain,while the helical C-terminal domain mediates dimer formation. Comparisonwith the CoA- and NAD+-bound human orthologue mitochondrial hydroxyacyl-CoA dehydrogenase shows extensive conservation of the residues that mediatesubstrate and cofactor binding. Superposition with the multi-catalytic homo-logue M. tuberculosis FadB, which forms a trifunctional complex with thethiolase FadA, indicates that FadB has developed structural features thatprevent its self-association as a dimer. Conversely, FadB2 is unable to substitutefor FadB in the tetrameric FadA-FadB complex as it lacks the N-terminalhydratase domain of FadB. Instead, FadB2 may functionally (or physically)associate with the enoyl-CoA hydratase EchA8 and the thiolases FadA2, FadA3,FadA4 or FadA6 as suggested by interrogation of the STRING protein-networkdatabase.
机译：细胞内病原体结核分枝杆菌结核病的病原体oftuberculosis,的一个主要原因全球死亡率。肺结核在宿主巨噬细胞长期persistencedepends时期,部分分解宿主细胞脂质作为碳源。这个机体分解代谢是强调theextensive冗余的基因在机会(approx100基因)。研究表明,结核分枝杆菌的酶学L-3-hydroxyacyl-CoAdehydrogenase FadB2是为特征。thisenzyme ligand-free形式报告2.1一项决议。有三个独特的二聚体复制/不对称单位。在氨基Rossmann-fold主题域,而螺旋c端域调和二聚体的形成。和人类orthologue线粒体NAD +绑定hydroxyacyl-CoA脱氢酶显示广泛的保护的残留mediatesubstrate和代数余子式绑定。叠加的multi-catalytic homo-logue结核分枝杆菌FadB,形成三功能性的复杂与thethiolase FadA,表明FadB发展结构特点thatprevent self-association作为一个二聚体。相反,FadB2无法substitutefor FadB在四聚物的FadA-FadB复杂的,因为它缺乏FadB N-terminalhydratase域。FadB2可能功能(或身体)联系起来与enoyl-CoA水合酶EchA8和建议通过审讯的字符串

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