Sato Hideyo, Nomura Shinobu, Maebara Kanako, Sato Kanako, Tamba Michiko, Bannai Shiro
Department of Biochemistry, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan.
Biochem Biophys Res Commun. 2004 Dec 3;325(1):109-16. doi: 10.1016/j.bbrc.2004.10.009.
Recent studies have demonstrated that depletion of amino acids results in the induction of several genes and that a genomic cis-element termed amino acid response element (AARE) is required for the induction. System x(c)(-) is an anionic amino acid transport system highly specific for cystine and glutamate, and its activity is known to be induced by cystine deprivation. This transporter is composed of two protein components, xCT and 4F2 heavy chain, and xCT is thought to mediate the transport activity. In the present study, the molecular mechanism for the induction of xCT by amino acid deprivation has been investigated. In mouse NIH3T3 cells, the activity of system x(c)(-) and xCT mRNA is induced not only by deprivation of cystine but also by deprivation of other amino acids. Two AAREs, each located in the opposite direction with an intervening sequence, were found in the 5'-flanking region of the mouse xCT gene. Promoter analysis revealed that both AAREs were necessary for the maximal induction of xCT mRNA in response to the amino acid deprivation. Glucose deprivation had no effect on the induction of the activity of system x(c)(-). Electrophoretic mobility shift assay showed that ATF4, but not ATF2, is involved in the amino acid control of xCT expression. These results demonstrate that xCT is a new member of the proteins whose transcriptional control by the amino acid deprivation is mediated by AARE.
最近的研究表明,氨基酸的缺乏会导致多个基因的诱导表达,并且这种诱导需要一个称为氨基酸反应元件(AARE)的基因组顺式元件。系统x(c)(-)是一种对胱氨酸和谷氨酸具有高度特异性的阴离子氨基酸转运系统,已知其活性可被胱氨酸剥夺所诱导。该转运体由两个蛋白质组分xCT和4F2重链组成,其中xCT被认为介导了转运活性。在本研究中,对氨基酸剥夺诱导xCT的分子机制进行了研究。在小鼠NIH3T3细胞中,系统x(c)(-)的活性和xCT mRNA不仅可被胱氨酸剥夺诱导,也可被其他氨基酸剥夺诱导。在小鼠xCT基因的5'侧翼区域发现了两个AARE,它们的方向相反且中间有间隔序列。启动子分析表明,这两个AARE对于响应氨基酸剥夺时xCT mRNA的最大诱导都是必需的。葡萄糖剥夺对系统x(c)(-)活性的诱导没有影响。电泳迁移率变动分析表明,参与xCT表达氨基酸调控的是ATF4,而非ATF2。这些结果表明,xCT是一类蛋白质的新成员,其转录调控是由AARE介导的氨基酸剥夺所介导的。