The Gcn2 kinase as a cell cycle regulator

The Gcn2 kinase as a cell cycle regulator
复制标题

DOI:
10.4161/cc.6.22.4933
复制
发表时间:
2007-11-15
期刊:
影响因子:
4.3
通讯作者:
Boye, Erik
Boye, Erik
中科院分区:
生物学3区
文献类型:
--
作者:
Grallert, Beata;Boye, Erik

文献摘要

被引文献

相似文献

通过G(1)期的细胞周期进展是特别重要的,因为这是决定开始另一个细胞周期的阶段。异常的G(1)/S转换通常导致细胞周期失调和癌症发展。因此,有一个复杂的调控网络,以确保及时进入S期,协调启动DNA复制与生长和压力信号。我们已经研究了裂变酵母细胞在G(1)期对紫外线(UV)照射的反应,并确定了一个Gcn 2依赖的检查点,延迟进入S期。紫外线照射激活Gcn 2,进而磷酸化翻译起始因子eIF 2 α并抑制翻译。eIF 2 α的磷酸化是一种众所周知的对各种形式的应激的反应,但这种反应是否或如何引起特定的细胞周期效应尚不清楚。在这里,我们讨论Gcn 2活性,eIF 2a磷酸化,翻译下调和细胞周期延迟之间的关系。
Cell cycle progression through G(1) phase is of particular importance because this is the phase where the decision to embark on another cell cycle is made. An aberrant G(1)/S transition often leads to cell cycle deregulation and cancer development. Therefore, there is a complex regulatory network to ensure timely entry into S phase, coordinating initiation of DNA replication with growth and stress signals. We have studied the response of fission yeast cells to ultraviolet (UV) irradiation in G(1) phase and identified a Gcn2-dependent checkpoint that delays entry into S phase. UV irradiation activates Gcn2 which, in turn, phosphorylates the translation initiation factor eIF2 alpha and depresses translation. Phosphorylation of eIF2 alpha is a well-known response to various forms of stress, but whether or how this response is causing the specific cell cycle effects is not known. Here we discuss the relationships between Gcn2 activity, eIF2a phosphorylation, translation downregulation and cell cycle delay.