Trichinella spiralis-infected muscle cells: abundant RNA polymerase II in nuclear speckle domains colocalizes with nuclear antigens.

Trichinella spiralis-infected muscle cells: abundant RNA polymerase II in nuclear speckle domains colocalizes with nuclear antigens.
复制标题

旋毛虫感染的肌肉细胞:核斑点域中丰富的 RNA 聚合酶 II 与核抗原共定位。

DOI:
10.1128/iai.69.6.4065-4071.2001
复制
发表时间:
2001
影响因子:
3.1
通讯作者:
Jasmer,DP
Jasmer,DP
中科院分区:
医学2区
文献类型:
--
作者:
Yao,C;Jasmer,DP

文献摘要

相似文献

旋毛虫感染哺乳动物骨骼肌细胞可导致宿主细胞核多倍体(约4N)并异常增大。据推测,这种扩增反映了感染诱导宿主转录的上调。经常用驱虫药治疗。用甲苯咪唑(MBZ)感染螺旋虫的啮齿动物可使感染的细胞核缩小,单个感染的肌肉细胞的总RNA含量显著减少。用抗RNA聚合酶II(POL II)大亚基的单抗研究了感染对分离的感染细胞核中POL II水平的影响。POL II定位于分离的感染细胞核中的斑点结构域。类似的结构域以前已经定位于RNA合成或加工的位置。与来自其他未感染宿主细胞的细胞核中的水平相比,斑点定位的POLII(SL-POLII)水平在感染的细胞核中显著升高,平均高出3.9到6.8倍。抗病毒抗体识别的核抗原(NA)。螺旋定位于受感染的细胞核。用共聚焦显微镜发现NA亚群与POL II定义的大部分斑点结构域共存。MBZ治疗慢性感染的小鼠,耗尽感染细胞核中的NA,导致感染细胞核中SL-POL II的显著耗尽。对照核的SL-Pol II平均比MBZ处理的核多70%。Pol II在这些多倍体细胞核中的平均残留水平比2N对照核中的水平高120%。这些观察可能表明感染对宿主细胞中POL II水平有两种不同的影响。
Infection of mammalian skeletal muscle cells byTrichinella spiraliscauses host nuclei to become polyploid (ca. 4N) and abnormally enlarged. It has been postulated that this enlargement reflects an infection-induced elevation of host transcription. Anthelmintic treatment ofT. spiralis-infected rodents with mebendazole (MBZ) causes a reduction in the size of infected cell nuclei and a significant reduction in the total RNA content of individual infected muscle cells. A monoclonal antibody to the large subunit of RNA polymerase II (Pol II) was used here to assess the effects of infection on Pol II levels in isolated infected cell nuclei. Pol II was localized to speckle domains in isolated infected cell nuclei. Similar domains have been previously localized to sites of RNA synthesis or processing. When compared to the levels in nuclei from other, uninfected host cells, speckle-localized Pol II (SL-Pol II) levels were significantly elevated in infected cell nuclei by a mean of 3.9- to 6.8-fold. Nuclear antigens (NA) recognized by antibodies againstT. spiralislocalized to infected cell nuclei. By use of confocal microscopy, a subpopulation of NA was found colocalized with most speckle domains defined by Pol II. MBZ treatment of chronically infected mice, which depletes NA from infected cell nuclei, caused a significant depletion of SL-Pol II from infected cell nuclei. Control nuclei had a mean of 70% more SL-Pol II than MBZ-treated nuclei. The mean residual level of Pol II in these polyploid nuclei remained elevated by 120% over the level in 2N control nuclei. These observations may indicate two distinct effects of infection on Pol II levels in host cells.