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首页> 外文期刊>Molecular and Cellular Biology >The Ras-specific exchange factors mouse Sos1 (mSos1) and mSos2 are regulated differently: mSos2 contains ubiquitination signals absent in mSos1.
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The Ras-specific exchange factors mouse Sos1 (mSos1) and mSos2 are regulated differently: mSos2 contains ubiquitination signals absent in mSos1.

机译：特定于Ras的交换因子小鼠Sos1（mSos1）和mSos2的调控方式不同：mSos2包含mSos1中不存在的泛素化信号。

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We have compared aspects of the mouse sos1 (msos1) and msos2 genes, which encode widely expressed, closely related Ras-specific exchange factors. Although an msos1 plasmid did not induce phenotypic changes in NIH 3T3 cells, addition of a 15-codon myristoylation signal to its 5' end enabled the resulting plasmid, myr-sos1, to induce approximately one-half as many foci of transformed cells as a v-H-ras control. By contrast, an isogenic myr-sos2 plasmid, which was made by fusing the first 102 codons from myr-sos1 at homologous sequences to an intact msos2 cDNA, did not induce focal transformation directly, although it could form foci in cooperation with c-H-ras. Pulse-chase experiments indicated that the half-life of Sos1 in NIH 3T3 cells was greater than 18 h, while that of Sos2 was less than 3 h. While in vitro-translated Sos1 was stable in a rabbit reticulocyte lysate, Sos2 was degraded in the lysate, as were each of two reciprocal chimeric Sos1-Sos2 proteins, albeit at a slower rate. In the lysate, Sos2 and the two chimeric proteins could be stabilized by ATPgammaS. Unlike Sos1, Sos2 was specifically immunoprecipitated by antiubiquitin antibodies. In a myristoylated version, the chimeric gene encoding Sos2 at its C terminus made a stable protein in NIH 3T3 cells and induced focal transformation almost as efficiently as myr-msos1, while the myristoylated protein encoded by the other chimera was unstable and defective in the transformation assay. We conclude that mSos2 is much less stable than mSos1 and is degraded by a ubiquitin-dependent process. A second mSos2 degradation signal, mapped to the C terminus in the reticulocyte lysate, does not seem to function under the growth conditions of the NIH 3T3 cells.
机译：我们比较了小鼠sos1（msos1）和msos2基因的各个方面，这些基因编码广泛表达的，密切相关的Ras特异性交换因子。尽管msos1质粒不会在NIH 3T3细胞中诱导表型变化，但在其5'端添加15个密码子肉豆蔻酰化信号，可使所得质粒myr-sos1诱导转化细胞的转化率约为转化的细胞的一半。 vH-ras控制。相比之下，同基因的myr-sos2质粒是通过将来自myr-sos1的前102个密码子同源序列融合到完整的msos2 cDNA而制成的，尽管它可以与cH-ras结合形成灶，但它并不能直接诱导病灶转化。 。脉冲追踪实验表明，Sos1在NIH 3T3细胞中的半衰期大于18 h，而Sos2在3H3T3细胞中的半衰期小于3 h。尽管体外翻译的Sos1在兔网织红细胞裂解物中稳定，但Sos2在裂解物中却被降解，两个互作嵌合的Sos1-Sos2蛋白也是如此，尽管速度较慢。在裂解物中，Sos2和两个嵌合蛋白可以被ATPgammaS稳定。与Sos1不同，Sos2被抗泛素抗体特异性免疫沉淀。在一个肉豆蔻酰化的版本中，在其C端编码Sos2的嵌合基因在NIH 3T3细胞中产生了稳定的蛋白质，并几乎与myr-msos1一样有效地诱导了病灶转化，而由另一种嵌合体编码的豆蔻酰化的蛋白质则不稳定且在转化中有缺陷分析。我们得出的结论是，mSos2的稳定性远不如mSos1，并且会因泛素依赖性过程而降解。第二个mSos2降解信号映射到网织红细胞裂解物中的C末端，在NIH 3T3细胞的生长条件下似乎不起作用。

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