Mechanism of membrane fluidityoptimization:: isothermal control of the Bacillus subtilis acyl-lipid desaturase
Mechanism of membrane fluidityoptimization:: isothermal control of the Bacillus subtilis acyl-lipid desaturase
复制标题
DOI：
10.1046/j.1365-2958.2002.03103.x
复制
发表时间：
2002-09-01
影响因子：
3.6
通讯作者：
de Mendoza, D
中科院分区：
文献类型：
--
作者：
Cybulski, LE;Albanesi, D;de Mendoza, D
枯草芽孢杆菌的Des途径调节酰基脂质去饱和酶Des的表达，从而控制从饱和磷脂前体合成不饱和脂肪酸（UFA）。以前，我们表明，主开关的DES途径是一个双组分的调节系统组成的膜相关激酶，DesK，和可溶性转录调节因子，DesR，严格控制DES基因的转录。当细胞转移到低生长温度时，该途径被激活。在这里，我们报告的机制，异亮氨酸调节Des途径。我们发现，外源异亮氨酸来源，以及其α-酮酸衍生物，这是一种支链脂肪酸的前体，负调控des基因的表达在37 degreesC。DesK-DesR双组分系统介导这种反应，因为需要两个伴侣在37 ℃下感知和识别异亮氨酸信号。脂肪酸谱强烈表明，异亮氨酸影响DesK传感器蛋白的信号传导状态，通过显着增加低熔点反异构支链脂肪酸掺入膜磷脂。我们认为，在恒定温度下膜流动性的降低和温度下降通过相同的机制诱导des。因此，Des途径将提供一种新的机制，以优化膜脂质流动性在恒定的温度。
The Des pathway of Bacillus subtilis regulates the expression of the acyl-lipid desaturase, Des, thereby controlling the synthesis of unsaturated fatty acids (UFAs) from saturated phospholipid precursors. Previously, we showed that the master switch for the Des pathway is a two-component regulatory system composed of a membrane-associated kinase, DesK, and a soluble transcriptional regulator, DesR, which stringently controls transcription of the des gene. Activation of this pathway takes place when cells are shifted to low growth temperature. Here, we report on the mechanism by which isoleucine regulates the Des pathway. We found that exogenous isoleucine sources,as well as its alpha-keto acid derivative, which is a branched-chain fatty acid precursor, negatively regulate the expression of the des gene at 37degreesC. The DesK-DesR two-component system mediates this response, as both partners are required to sense and transduce the isoleucine signal at 37degreesC. Fatty acid profiles strongly indicate that isoleucine affects the signalling state of the DesK sensor protein by dramatically increasing the incorporation of the lower-melting-point anteiso-branched-chain fatty acids into membrane phospholipids. We propose that both a decrease in membrane fluidity at constant temperature and a temperature downshift induce des by the same mechanism. Thus, the Des pathway would provide a novel mechanism to optimize membrane lipid fluidity at a constant temperature.