Fukasawa K, Murakami M S, Blair D G, Kuriyama R, Hunt T, Fischinger P, Vande Woude G F
ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201.
Cell Growth Differ. 1994 Oct;5(10):1093-103.
The mos protooncogene encodes a serine/threonine kinase and is a key regulator of oocyte meiotic maturation. After acute infection of Swiss 3T3 cells with virus containing the v-mos oncogene, cells expressing high levels of v-Mos round up and detach from the monolayer (floating cells), while cells that remain attached express 10-fold lower levels of v-Mos and are transformed. The floating cells are growth arrested with their chromosomes partially condensed in the absence of histone H1 kinase activity, while mitogen-activated protein kinase activity is very high. Collectively, these properties are similar to properties observed in maturing oocytes between meiosis I and II. In v-mos-transformed cell populations, mitogen-activated protein kinase activity is also elevated, correlating with the degree of morphological transformation and the level of Mos expression. Moreover, phosphoprotein modifications specific for M are found in both the floating cells and in v-mos-transformed cells, regardless of their cell cycle stage. One explanation for both morphological transformation and the phenotypes of the floating cells is that Mos imposes a meiotic program on different stages of the somatic cell cycle. The extent of this meiotic phenotype is proportional to the level of v-Mos expression. These results suggest that both morphological transformation and the phenotypes of the floating cells induced by Mos in Swiss 3T3 cells are related to its normal activities during oocyte maturation.
mos原癌基因编码一种丝氨酸/苏氨酸激酶,是卵母细胞减数分裂成熟的关键调节因子。用含有v-mos癌基因的病毒急性感染瑞士3T3细胞后,高表达v-Mos的细胞会变圆并从单层细胞上脱离(漂浮细胞),而仍附着的细胞v-Mos表达水平低10倍且发生了转化。漂浮细胞生长停滞,其染色体在没有组蛋白H1激酶活性的情况下部分浓缩,而丝裂原活化蛋白激酶活性非常高。总体而言,这些特性与在减数分裂I和II之间成熟卵母细胞中观察到的特性相似。在v-mos转化的细胞群体中,丝裂原活化蛋白激酶活性也升高,这与形态转化程度和Mos表达水平相关。此外,无论细胞周期阶段如何,在漂浮细胞和v-mos转化细胞中都发现了对M特异的磷蛋白修饰。对形态转化和漂浮细胞表型的一种解释是,Mos将减数分裂程序强加于体细胞周期的不同阶段。这种减数分裂表型的程度与v-Mos表达水平成正比。这些结果表明,Mos在瑞士3T3细胞中诱导的形态转化和漂浮细胞表型均与其在卵母细胞成熟过程中的正常活性有关。