FrsA functions as a cofactor-independent decarboxylase to control metabolic flux
FrsA functions as a cofactor-independent decarboxylase to control metabolic flux
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DOI：
10.1038/nchembio.589
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发表时间：
2011-07-01
影响因子：
14.8
通讯作者：
Cha, Sun-Shin
中科院分区：
文献类型：
--
作者：
Lee, Kyung-Jo;Jeong, Chang-Sook;Cha, Sun-Shin
发酵呼吸开关(FRSA)蛋白与葡萄糖专一性酶IIA(GLC)的相互作用促进了葡萄糖在氧气限制条件下的发酵。我们发现，FRSA以辅因子不依赖的方式将丙酮酸转化为乙醛和二氧化碳，其丙酮酸脱羧基活性被IIA(GLC)(d-IIA(GLC))的去磷酸化形式增强。FRSA及其与d-IIA(GLC)络合物的晶体结构揭示了催化所需的残基以及d-IIA(GLC)活化的结构基础。
The interaction between fermentation-respiration switch (FrsA) protein and glucose-specific enzyme IIA(Glc) increases glucose fermentation under oxygen-limited conditions. We show that FrsA converts pyruvate to acetaldehyde and carbon dioxide in a cofactor-independent manner and that its pyruvate decarboxylation activity is enhanced by the dephosphorylated form of IIA(Glc) (d-IIA(Glc)). Crystal structures of FrsA and its complex with d-IIA(Glc) revealed residues required for catalysis as well as the structural basis for the activation by d-IIA(Glc).