Zou Qi, Dong Huijuan, Zhu Lei, Cronan John E
Department of Biochemistry, University of Illinois at Urbana-Champaign, Urbana, IL, United States.
Department of Microbiology, University of Illinois at Urbana-Champaign, Urbana, IL, United States.
Front Microbiol. 2022 Apr 25;13:877582. doi: 10.3389/fmicb.2022.877582. eCollection 2022.
The phospholipid acyl chains of can be derived either by synthesis or by incorporation of exogenous fatty acids through the fatty acid kinase complex (Fak)-phosphate acyltransferase (PlsX) pathway. Exogenous fatty acids suppress fatty acid synthesis through the transcriptional repressor FabT, the loss of which eliminated regulation of fatty acid biosynthesis and resulted in decreased incorporation of exogenous unsaturated fatty acids. Purified FabT bound to the promoters of several fatty acid synthesis genes that contain a specific palindromic sequence and binding was enhanced by acylated derivatives of acyl carrier protein B (acyl-AcpB). The loss of the PlsX pathway blocked FabT-dependent transcriptional repression in the presence of oleic acid. Transcriptional repression was partially retained in a Δ strain which showed decreased fatty acid biosynthesis in the presence of exogenous unsaturated fatty acids. The FabT-dependent activity remaining in the Δ strain indicates that acylated derivatives of AcpA were weak enhancers of FabT binding although AcpA is believed to primarily function in fatty acid synthesis.
的磷脂酰链可以通过合成或通过脂肪酸激酶复合物（Fak）-磷酸酰基转移酶（PlsX）途径掺入外源脂肪酸来获得。外源脂肪酸通过转录阻遏物FabT抑制脂肪酸合成，FabT的缺失消除了脂肪酸生物合成的调控，并导致外源不饱和脂肪酸掺入减少。纯化的FabT与几个含有特定回文序列的脂肪酸合成基因的启动子结合，酰基载体蛋白B的酰化衍生物（酰基-AcpB）增强了这种结合。在油酸存在下，PlsX途径的缺失阻断了FabT依赖的转录抑制。在存在外源不饱和脂肪酸时显示脂肪酸生物合成减少的Δ菌株中，转录抑制部分保留。Δ菌株中剩余的FabT依赖活性表明，尽管认为AcpA主要在脂肪酸合成中起作用，但AcpA的酰化衍生物是FabT结合的弱增强剂。
