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在果蝇中,细胞周期蛋白E水平的波动是多轮内复制周期S期所必需的。

Fluctuations in cyclin E levels are required for multiple rounds of endocycle S phase in Drosophila.

作者信息

Follette P J, Duronio R J, O'Farrell P H

机构信息

Department of Biochemistry and Biophysics, University of California, San Francisco 94143-0448, USA.

出版信息

Curr Biol. 1998 Feb 12;8(4):235-8. doi: 10.1016/s0960-9822(98)70089-2.

Abstract

The precise cell-cycle alternation of S phase and mitosis is controlled by alternating competence of nuclei to respond to S-phase-inducing factors [1]. Nuclei acquire competence to replicate at the low point in cyclin-dependent kinase (Cdk) activities that follows mitotic destruction of cyclins. The elevation of Cdk activity late in G1 is thought to drive cells into S phase and to block replicated DNA from re-acquiring replication competence [2]. Whereas mitosis is normally required to eliminate the cyclins prior to another cycle of replication, experimental elimination of Cdk activity in G2 can restore competence to replicate [3-6]. Here, we examine the roles of Cdks in the endocycies of Drosophila [7]. In these cycles, rounds of discrete S phases without intervening mitoses result in polyteny. Cyclins A and B are lost in cells as they enter endocycles [8,9], and pulses of Cyclin E expression drive endocycle S phases [10-12]. To address whether oscillations of Cyclin E expression are required for endocycles, we expressed Cyclin E continuously in Drosophila salivary glands. Growth of the cells was severely inhibited, and a period of DNA replication was induced but further replication was inhibited. This replication inhibition could be overcome by the kinase inhibitor 6-dimethylaminopurine (6-DMAP), but not by expression of subunits of the transcription factor E2F. These results indicate that endocycle S phases require oscillations in Cdk activity, but, in contrast to oscillations in mitotic cells, these occur independently of mitosis.

摘要

S期和有丝分裂精确的细胞周期交替是由细胞核对S期诱导因子作出反应的交替能力所控制的[1]。细胞核在细胞周期蛋白依赖性激酶(Cdk)活性的最低点获得复制能力,该最低点出现在细胞周期蛋白在有丝分裂时被破坏之后。G1晚期Cdk活性的升高被认为会驱动细胞进入S期,并阻止复制后的DNA重新获得复制能力[2]。虽然通常需要有丝分裂来在另一个复制周期之前消除细胞周期蛋白,但在G2期实验性地消除Cdk活性可以恢复复制能力[3 - 6]。在这里,我们研究了Cdk在果蝇内复制周期中的作用[7]。在这些周期中,一轮轮离散的S期而没有中间的有丝分裂会导致多线化。细胞进入内复制周期时,细胞周期蛋白A和B会丢失[8,9],细胞周期蛋白E表达的脉冲驱动内复制周期的S期[10 - 12]。为了探究细胞周期蛋白E表达的振荡对于内复制周期是否必要,我们在果蝇唾液腺中持续表达细胞周期蛋白E。细胞生长受到严重抑制,诱导了一段DNA复制时期,但进一步的复制被抑制。这种复制抑制可以被激酶抑制剂6 - 二甲基氨基嘌呤(6 - DMAP)克服,但不能通过转录因子E2F亚基的表达来克服。这些结果表明,内复制周期的S期需要Cdk活性的振荡,但与有丝分裂细胞中的振荡不同,这些振荡独立于有丝分裂发生。

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