Gurvitz Aner
Section of Physiology of Lipid Metabolism, Center for Physiology, Pathophysiology and Immunology, Institute of Physiology, Medical University of Vienna, Schwarzspanierstrasse 17, 1090 Vienna, Austria.
Comp Funct Genomics. 2009;2009:836172. doi: 10.1155/2009/836172. Epub 2009 Oct 21.
Mycobacterium tuberculosis mtFabD is an essential malonyl-CoA:AcpM transacylase and is important for vital protein-protein interactions within type 2 fatty acid synthase FASII. mtFabD contacts KasA, KasB, FabH, InhA, and possibly also HadAB, HadBC, and FabG1/MabA. Disruption of mtFabD's interactions during FASII has been proposed for drug development. Here, the gene for a mitochondrially targeted mtFabD was ectopically expressed in Saccharomyces cerevisiae mct1Delta mutant cells lacking the corresponding mitochondrial malonyl-CoA transferase Mct1p, allowing the mutants to recover their abilities to respire on glycerol and synthesize lipoic acid. Hence, mtFabD could physiologically function in an environment lacking holo-AcpM or other native interaction partners.
结核分枝杆菌的mtFabD是一种必需的丙二酰辅酶A：AcpM转酰基酶，对2型脂肪酸合酶FASII内的重要蛋白质-蛋白质相互作用至关重要。mtFabD与KasA、KasB、FabH、InhA接触，也可能与HadAB、HadBC和FabG1/MabA接触。有人提出，在FASII过程中破坏mtFabD的相互作用可用于药物开发。在这里，线粒体靶向的mtFabD基因在缺乏相应线粒体丙二酰辅酶A转移酶Mct1p的酿酒酵母mct1Delta突变细胞中异位表达，使突变体恢复了在甘油上呼吸和合成硫辛酸的能力。因此，mtFabD可以在缺乏全酶形式的AcpM或其他天然相互作用伙伴的环境中发挥生理功能。
