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首页> 外文期刊>Molecular and Cellular Biology >Two classes of mutant mammary tumor virus-infected HTC cell with defects in glucocorticoid-regulated gene expression.
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Two classes of mutant mammary tumor virus-infected HTC cell with defects in glucocorticoid-regulated gene expression.

机译：两类突变的乳腺肿瘤病毒感染的HTC细胞在糖皮质激素调节的基因表达中存在缺陷。

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We have isolated mutant derivatives of M1.54 (a mammary tumor virus [MTV]-infected rat hepatoma [HTC] cell line containing multiple integrated proviruses) that fail to express hormone-inducible cell surface viral glycoproteins. In wild-type M1.54, the synthetic glucocorticoid dexamethasone selectively stimulates the rate of synthesis of MTV RNA. In addition, dexamethasone is essential for posttranslational maturation of three of the four cell surface viral glycoproteins processed from the MTV glycosylated precursor polyprotein; the fourth mature species is produced constitutively. Two mutant phenotypes are described; each contains glucocorticoid receptors that are indistinguishable from the wild-type receptor with respect to hormone affinity, intracellular concentration, nuclear translocation efficiency, DNA-cellulose chromatography, and sedimentation rate. In one class, represented by the mutant line CR1, dexamethasone fails to stimulate the low basal rate of MTV gene transcription; surprisingly, hormonal regulation of tyrosine aminotransferase activity is also defective in CR1, whereas several other cellular responses to dexamethasone are normal. In the second class of mutants, represented by CR4, dexamethasone stimulates synthesis of MTV transcripts indistinguishable from those produced in M1.54, but only the constitutive cell surface viral glycoprotein is expressed. Thus, these mutants define two distinct and novel aspects of glucocorticoid regulated gene expression in HTC cells: CR4 contains a defect in a hormone inducible protein maturation pathway that acts on specific viral (and presumably cellular) precursor polypeptides, whereas the lesion in CR1 appears to affect the expression of a subset of the gene products normally under glucocorticoid control in M1.54.
机译：我们已分离出无法表达激素诱导型细胞表面病毒糖蛋白的M1.54（感染了乳腺肿瘤病毒[MTV]的大鼠肝癌[HTC]细胞系，含有多种整合的原病毒）的突变衍生物。在野生型M1.54中，合成的糖皮质激素地塞米松选择性刺激MTV RNA的合成速率。此外，地塞米松对于从MTV糖基化前体多蛋白加工的四个细胞表面病毒糖蛋白中的三个糖蛋白的翻译后成熟至关重要。第四成熟种是组成性产生的。描述了两种突变型。每个都含有糖皮质激素受体，就激素亲和力，细胞内浓度，核转运效率，DNA纤维素色谱法和沉降速率而言，它们与野生型受体没有区别。在以突变株CR1为代表的一类中，地塞米松不能刺激低基础率的MTV基因转录。令人惊讶的是，CR1中酪氨酸氨基转移酶活性的激素调节也有缺陷，而对地塞米松的其他几种细胞反应是正常的。在以CR4为代表的第二类突变体中，地塞米松刺激与M1.54中产生的MTV转录物无法区分的MTV转录物的合成，但仅表达组成型细胞表面病毒糖蛋白。因此，这些突变体定义了HTC细胞中糖皮质激素调节基因表达的两个不同而新颖的方面：CR4在激素诱导的蛋白质成熟途径中包含一个缺陷，该途径作用于特定的病毒（可能是细胞）前体多肽，而CR1中的病变似乎影响在M1.54中通常受糖皮质激素控制的基因产物子集的表达。

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