LSU Digital Commons LSU Digital Commons Coordination of ribosomal protein and ribosomal RNA gene Coordination of ribosomal protein and ribosomal RNA gene expression in response to TOR signaling expression in response to TOR signaling

LSU Digital Commons LSU Digital Commons Coordination of ribosomal protein and ribosomal RNA gene Coordination of ribosomal protein and ribosomal RNA gene expression in response to TOR signaling expression in response to TOR signaling
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:细胞生长是对营养或生长因子的反应,这些营养或生长因子的存在是通过弹性速率信号通路检测和传递的。蛋白激酶在细胞周期进程和基因表达等过程中起着至关重要的作用,而这些通路的错误调控与各种疾病状态有关。旨在促进细胞生长的信号会聚在核糖体生物发生上,因为产生细胞蛋白的能力与细胞生长密切相关。因此,对生长信号的部分反应是编码核糖体RNA(RRNA)和核糖体蛋白(Rp)的基因的协调表达。调节细胞生长的一个关键因素是雷帕霉素(TOR)激酶的靶标,它是在营养应激条件下阻止细胞周期从G1向S进展的守门人之一。Tor在所有真核生物中在结构和功能上都是保守的。在有利的生长条件下,TOR是活跃的,细胞保持着强劲的核糖体生物发生、翻译启动和营养输入的速度。在应激条件下,TOR信号被抑制,导致细胞周期停滞,而TOR不能对环境或营养信号做出适当的反应,导致细胞生长失控。来自酿酒酵母的新证据表明,高迁移率组(High Mobility Group,HMGB)蛋白是一种非序列特异的染色体蛋白,参与调节对生长信号的反应。由于HMGB蛋白具有改变DNA拓扑结构的能力,因此它们经常在高阶核蛋白复合体的组装中发挥作用。我们在这里回顾了最近的证据,这些证据表明HMGB蛋白可能功能协调依赖于TOR的rRNA和RP基因表达的调节。在国际人道主义法协会的地点。当TORC1激活时,共激活因子IFH1与FHL1结合,激活RP基因转录。当TORC1失活时,磷酸化的CRF1移位到细胞核,与IFH1竞争结合FHL1并抑制转录。在也含有Utp22、Rrp7和CKII的“Curi”复合体中发现了IFH1,FHL1也与之相关。在TORC1失活时,HMO1从这两类基因中解离。
: Cells grow in response to nutrients or growth factors, whose presence is detected and communicated by elabo-rate signaling pathways. Protein kinases play crucial roles in processes such as cell cycle progression and gene expression, and misregulation of such pathways has been correlated with various diseased states. Signals intended to promote cell growth converge on ribosome biogenesis, as the ability to produce cellular proteins is intimately tied to cell growth. Part of the response to growth signals is therefore the coordinate expression of genes encoding ribosomal RNA (rRNA) and ribosomal proteins (RP). A key player in regulating cell growth is the Target of Rapamycin (TOR) kinase, one of the gate-keepers that prevent cell cycle progression from G1 to S under conditions of nutritional stress. TOR is structurally and functionally conserved in all eukaryotes. Under favorable growth conditions, TOR is active and cells maintain a robust rate of ribosome biogenesis, translation initiation and nutrient import. Under stress conditions, TOR signaling is sup-pressed, leading to cell cycle arrest, while the failure of TOR to respond appropriately to environmental or nutritional signals leads to uncontrolled cell growth. Emerging evidence from Saccharomyces cerevisiae indicates that High Mobility Group (HMGB) proteins, non-sequence-specific chromosomal proteins, participate in mediating responses to growth signals. As HMGB proteins are distinguished by their ability to alter DNA topology, they frequently function in the assembly of higher-order nucleoprotein complexes. We review here recent evidence, which suggests that HMGB proteins may function to coordinate TOR-dependent regulation of rRNA and RP gene expression. at IFHL sites. When TORC1 is active, the coactivator IFH1 binds FHL1 to activate RP gene transcription. When TORC1 is inactive, phosphorylated CRF1 translocates to the nucleus to compete with IFH1 for binding to FHL1 and repress transcription. IFH1 is found in the “CURI” complex also containing Utp22, Rrp7, and CKII, with which FHL1 also associates. HMO1 dissociates from both classes of genes on inactivation of TORC1.