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红细胞前体细胞系中全球蛋白染色质结构的温度敏感变化被ts-AEV转化为ts-AEV

H Weintraub, H Beug, M Groudine

|April 1, 1982

概括

在细胞中对温度敏感的鸟类红质母细胞瘤病毒 (AEV) 感染会阻止血红蛋白的产生. 在更高的温度下重新激活AEV转化基因 (erb),恢复血红蛋白合成并改变染色质结构.

科学领域:

分子生物学分子生物学
细胞生物学细胞生物学
遗传学是一个遗传学.

背景情况:

鸟类红细胞母细胞病毒 (AEV) 是一种致癌逆转录病毒,会感染造血细胞.
血球蛋白合成是红色球体分化的一个关键标志物.
对温度敏感的AEV突变允许通过温度变化研究病毒基因功能.

研究的目的:

研究AEV转化基因 (erb) 在调节血红蛋白生产中的作用.
检查病毒基因失活,血红蛋白合成和染色质结构之间的关系.
为了确定染色质的变化是否在全球蛋白基因的转录激活之前或之后.

主要方法:

在体外培养的骨髓细胞感染温度敏感AEV突变.
温度变化 (36°C至42°C),使病毒 erb 基因产物失活.
对血红蛋白生产和全球蛋白mRNA水平的分析.
在全球蛋白基因域中评估DNAase I过敏位点和DNA甲基化模式.

主要成果:

在AEV感染的细胞中42°C的erb基因失活诱导了血红蛋白的产生.
这种表型转换与阿尔法和β环球蛋白mRNA的增加有关.
观察到染色体的变化,包括DNAase I过敏部位和改变的DNA甲基化,其中有一些先前的血红蛋白表达.

结论:

在AEV erb基因产品积极抑制血红蛋白合成.
染色体结构的变化,例如DNAase I过敏位,可以在全球蛋白基因的转录激活之前发生.
全球蛋白染色质的结构性质可以独立确定,不一定一定与活性转录相关.

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