Jackson P, Bellett A J
J Virol. 1985 Sep;55(3):644-50. doi: 10.1128/JVI.55.3.644-650.1985.
The actin microfilament organization in rat embryo cells was examined by fluorescence microscopy with 7-nitrobenz-2-oxa-1,3-diazole-phallacidin and by electron microscopy, after mock infection or infection with adenovirus type 5 (Ad5). Infected cells showed severely reduced numbers of actin microfilaments and stress fibers, detectable early after infection. Mutants defective in Ad5 early genes were used to show that reduced microfilament organization was a function of the Ad5 transformation early gene 1a (E1a) and did not require expression of any other viral gene. The product of the E1a 13s mRNA was essential for the effect, although the 12s mRNA product appeared to contribute. Ad5 infection of the cells had no observable effect on total cell actin levels or on the ratio of monomeric to polymeric actin. E1a, therefore, affected only the higher-order organization of actin.
在用7-硝基苯-2-恶唑-1,3-二氮杂萘-鬼笔环肽进行荧光显微镜检查以及电子显微镜检查后,研究了模拟感染或感染5型腺病毒(Ad5)后大鼠胚胎细胞中的肌动蛋白微丝组织。感染的细胞显示肌动蛋白微丝和应力纤维的数量严重减少,在感染后早期即可检测到。利用Ad5早期基因缺陷的突变体表明,微丝组织减少是Ad5转化早期基因1a(E1a)的作用,不需要任何其他病毒基因的表达。E1a 13s mRNA的产物对该效应至关重要,尽管12s mRNA产物似乎也有贡献。细胞感染Ad5对总细胞肌动蛋白水平或单体肌动蛋白与聚合肌动蛋白的比例没有可观察到的影响。因此,E1a仅影响肌动蛋白的高级组织。