Jackson P, Bellett A J
Division of Virology and Cellular Pathology, John Curtin School of Medical Research, Australian National University, Canberra.
J Virol. 1989 Jan;63(1):311-8. doi: 10.1128/JVI.63.1.311-318.1989.
Flow cytometry and staining with 7-nitrobenz-2-oxa-1,3-diazole-phallacidin were used to investigate organization of the actin cytoskeleton in rat embryo cells at different stages of normal and adenovirus E1A-induced cell cycles. In uninfected cells in G0-G1 and S phases, actin was predominantly in the form of stress fibers. In G2, this organization changed to peripheral rings of thin filaments, while during mitosis, actin had a diffuse distribution. Infection of quiescent rat cells by adenovirus caused them to enter the cell cycle and replicate DNA and also caused disruption of stress fibers. Rapid disappearance of stress fibers and the appearance of peripheral rings of actin filaments began from 13 h after infection and closely followed synthesis of the E1A proteins. Infected cells began S phase at about 24 h after infection, and cells in G2 and mitosis were seen from 30 to 50 h. Thus, disruption of the actin cytoskeleton is an early effect of E1A and not an indirect consequence of the entry of infected cells into the cell cycle.
运用流式细胞术以及用7-硝基苯-2-恶唑-1,3-二氮杂萘-鬼笔环肽进行染色,来研究正常及腺病毒E1A诱导的细胞周期不同阶段大鼠胚胎细胞中肌动蛋白细胞骨架的组织情况。在处于G0-G1期和S期的未感染细胞中,肌动蛋白主要呈应力纤维的形式。在G2期,这种组织形式转变为细丝状的外周环,而在有丝分裂期间,肌动蛋白呈弥散分布。腺病毒感染静止的大鼠细胞会使其进入细胞周期并复制DNA,同时还会导致应力纤维的破坏。应力纤维的迅速消失以及肌动蛋白丝外周环的出现始于感染后13小时,并紧跟E1A蛋白的合成。受感染细胞在感染后约24小时开始进入S期,在30至50小时可见处于G2期和有丝分裂期的细胞。因此,肌动蛋白细胞骨架的破坏是E1A的早期效应,而非受感染细胞进入细胞周期的间接结果。