Wood W I, Peterson D O, Bloch K
J Biol Chem. 1977 Aug 25;252(16):5745-9.
The initial steady state rate and product distribution of fatty acid synthesis catalyzed by Mycobacterium smegmatis fatty acid synthetase has been investigated as a function of various concentrations of acetyl-CoA, malonyl-CoA, mycobacterial polysaccharide, and bovine serum albumin. Polysaccharide has a large effect on both rate and chain length. The steady state rate stimulation by polysaccharide is not duplicated by other acyl-CoA-binding molecules such as bovine serum albumin. It is concluded that relief of product inhibition does not adequately explain the specific effects of the mycobacterial polysaccharide. A general mechanism is presented which accounts for variations in reaction rate and produce pattern over a wide range of experimental conditions. We propose that the diffusion of long chain acyl-CoA (C14 to C24) from the enzyme is the rate-limiting step in fatty acid synthesis catalyzed by the M. smegmatis synthetase. Polysaccharide facilitates this rate-limiting step by forming a ternary complex with enzyme-bound acyl-CoA causing rapid release of product.
耻垢分枝杆菌脂肪酸合成酶催化的脂肪酸合成的初始稳态速率和产物分布已作为各种浓度的乙酰辅酶A、丙二酸单酰辅酶A、分枝杆菌多糖和牛血清白蛋白的函数进行了研究。多糖对速率和链长都有很大影响。多糖对稳态速率的刺激不能被其他酰基辅酶A结合分子如牛血清白蛋白所复制。得出的结论是，产物抑制的缓解并不能充分解释分枝杆菌多糖的特定作用。提出了一种通用机制，该机制解释了在广泛的实验条件下反应速率和产物模式的变化。我们提出，长链酰基辅酶A（C14至C24）从酶中的扩散是耻垢分枝杆菌合成酶催化的脂肪酸合成中的限速步骤。多糖通过与酶结合的酰基辅酶A形成三元复合物，促进这一限速步骤，从而导致产物的快速释放。
