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埃氏腹水瘤细胞感染脑心肌炎病毒后组蛋白H1微观不均一性的变化。

Changes in the microheterogeneity of histone H1 after mengovirus infection of Ehrlich ascites tumor cells.

作者信息

Traub U, Traub P

出版信息

Hoppe Seylers Z Physiol Chem. 1978 May;359(5):581-9. doi: 10.1515/bchm.1978.359.1.581.

Abstract

Employing high-resolution polyacryl-amide gradient slab-gel electrophoresis in 6M urea and 6% acetic acid, a distinct change in the microheterogeneity of histone H1 was detected after mengovirus infection of Ehrlich ascites tumor cells. Whereas in uninfected cells the band multiplicity was found to be 6, it was reduced to 4 in the course of the infectious cycle (8 to 9 h). It could be deomonstrated that, while the electrophoretically slowly moving subspecies H1e and H1f disappeared from the band profile of histone H1, the faster migrating bands H1a and H1b increased in relative intensity. The relative intensity of band H1d was also drastically reduced, that of band H1c stayed practically constant throughout infection. When Ehrlich ascites tumor cells were labeled with a mixture of [14C]amino acids prior to mengovirus infection, the radioactivity incorporated into histone H1 subspecies of low electrophoretic mobility was chased into histone H1 components of high mobility in the course of infection, suggesting a virus-induced, unidirectional interconversion of the multiple histone H1 subunits. With the exception of a histone H2B subspecies, which also decreased in amount, the relative quantities of the other histones stayed constant throughout infection.

摘要

在6M尿素和6%乙酸中采用高分辨率聚丙烯酰胺梯度平板凝胶电泳,发现在脑心肌炎病毒感染艾氏腹水瘤细胞后,组蛋白H1的微观不均一性发生了明显变化。在未感染的细胞中,条带多样性为6条,而在感染周期(8至9小时)中减少到4条。可以证明,虽然电泳迁移较慢的亚类H1e和H1f从组蛋白H1的条带图谱中消失,但迁移较快的条带H1a和H1b的相对强度增加。条带H1d的相对强度也大幅降低,条带H1c的相对强度在整个感染过程中基本保持不变。当艾氏腹水瘤细胞在脑心肌炎病毒感染前用[14C]氨基酸混合物标记时,在感染过程中,掺入低电泳迁移率组蛋白H1亚类的放射性被追踪到高迁移率的组蛋白H1组分中,这表明病毒诱导了多个组蛋白H1亚基的单向相互转化。除了一种含量也减少的组蛋白H2B亚类外,其他组蛋白的相对量在整个感染过程中保持不变。

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