Growth-associated gene expression is not constant in cells traversing G-1 after exiting mitosis.

Growth-associated gene expression is not constant in cells traversing G-1 after exiting mitosis.
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在退出有丝分裂后穿越 G-1 的细胞中,生长相关基因的表达并不稳定。

DOI:
10.1002/jcp.1041470207
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发表时间:
1991
影响因子:
5.6
通讯作者:
Soprano,KJ
Soprano,KJ
中科院分区:
生物学2区
文献类型:
--
作者:
Cosenza,SC;Carter,R;Pena,A;Donigan,A;Borrelli,M;Soprano,DR;Soprano,KJ

文献摘要

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分析生长停滞细胞刺激后的基因表达已成为鉴定生长相关基因的主要方法。由于这些基因序列的激活取决于刺激剂和细胞静止状态,因此相同基因的激活和作用在非生长停滞、活跃增殖的细胞中可能完全不同。我们通过分析刚退出有丝分裂而没有首先离开细胞周期的细胞在G-1期间的基因表达,解决了活跃生长期间生长相关基因表达的问题。我们能够通过非诱导、无药物系统分离出一群在有丝分裂中高度同步化的Swiss 3 T3细胞(>90%),其数量足以确定大量代表性生长相关基因的表达模式。我们的结果表明,在将有丝分裂细胞重新接种到条件培养基中后:(1)在活跃增殖细胞的G-I期间,生长相关基因表达不是恒定的,以及(2)虽然许多基因(例如,JE、c-myc、ODC、p53和组蛋白)表现出与静止系统中报道的相似的表达模式,其他(例如,努尔-77、波形蛋白、钙周期蛋白)表现出完全不同的模式。根据这些结果,我们可以开始构建活跃生长期间G-1进展的时间图。
Analysis of gene expression following stimulation of growth‐arrested cells has beei the main approach for identification of growth‐associated genes. Since the activation of these gene sequences is dependent on both the stimulatory agent and theitate of quiescence of the cell, the activation and role of the same genes may be entirely different in non‐growth arrested, actively proliferating cells. We have addressed the question of growth‐associated gene expression during active growth by analyzing gene expression during G‐1 of cells which have jusl exited mitosis without first leaving the cell cycle. We were able to isolate, by a non‐inductive, drug free system, a population of highly synchronized Swiss 3T3 cells within mitos is (>90%) in numbers sufficient to determine the pattern of expression pf a large number of representative growth‐associated genes. Our results show that after replating the mitotic ceils into conditioned medium: (1) growth‐associated gene expression is not constant during G‐1 of actively proliferating cells, and (2) while a number of genes (e.g., JE, c‐myc, ODC, p53, and histone) exhibited patterns of expression similar to that reported in the quiescent systems, others (e.g., nur‐77, vimentin, calcyclin) exhibited patterns which were completely different. From these results, we can begin to construct a temporal map of G‐1 progression during active growth.