Coupling of cell division to cell growth by translational control of the G(1) cyclin CLN3 in yeast
Coupling of cell division to cell growth by translational control of the G(1) cyclin CLN3 in yeast
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DOI：
10.1101/gad.11.19.2522
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发表时间：
1997-10-01
影响因子：
10.5
通讯作者：
Schmidt, EV
中科院分区：
文献类型：
--
作者：
Polymenis, M;Schmidt, EV
真核细胞周期由一系列细胞周期蛋白和激酶伴侣（包括酵母中的 G(1) 细胞周期蛋白 Cln3p）驱动。作为该级联的第一步，Cln3p 具有独特的定位，可以确定分裂的临界生长速率阈值。为了分析调节 CLN3 表达的因素，我们在 CLN3 mRNA 5' 前导区中鉴定了一个短上游开放阅读框（uORF）作为翻译控制元件。该控制元件对于 Cln3p 合成的生长依赖性调节至关重要，因为它在蛋白质合成减少或生长缓慢的条件下特异性抑制 CLN3 表达。 uORF 的失活加速了 Start 的完成并进入下降周期，表明 CLN3 的翻译调控提供了耦合细胞生长和分裂的机制。
The eukaryotic cell cycle is driven by a cascade of cyclins and kinase partners including the G(1) cyclin Cln3p in yeast. As the first step in this cascade, Cln3p is uniquely positioned to determine the critical growth-rate threshold for division. To analyze factors regulating CLN3 expression, we identified a short upstream open reading frame (uORF) in the 5' leader of CLN3 mRNA as a translational control element. This control element is critical for the growth-dependent regulation of Cln3p synthesis because it specifically represses CLN3 expression during conditions of diminished protein synthesis or slow growth. Inactivation of the uORF accelerates the completion of Start and entry into the fell cycle suggesting that translational regulation of CLN3 provides a mechanism coupling cell growth and division.