期刊
MOLECULAR BIOLOGY OF THE CELL
卷 20, 期 7, 页码 2070-2082出版社
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E08-02-0108
关键词
-
类别
资金
- Deutsche Forschungsgemeinschaft [Ri 828/5-2, SPP1128, Li 406/5-3]
- Volkswagen Foundation
- EU [LSHC-CT-2004-502943]
- Deutsche Krebshilfe
- Tumorzentrum Mannheim-Heidelberg
Telomerase-negative tumor cells maintain their telomeres via an alternative lengthening of telomeres (ALT) mechanism. This process involves the association of telomeres with promyelocytic leukemia nuclear bodies (PML-NBs). Here, the mobility of both telomeres and PML-NBs as well as their interactions were studied in human U2OS osteosarcoma cells, in which the ALT pathway is active. A U2OS cell line was constructed that had lac operator repeats stably integrated adjacent to the telomeres of chromosomes 6q, 11p, and 12q. By fluorescence microscopy of autofluorescent LacI repressor bound to the lacO arrays the telomere mobility during interphase was traced and correlated with the telomere repeat length. A confined diffusion model was derived that describes telomere dynamics in the nucleus on the time scale from seconds to hours. Two telomere groups were identified that differed with respect to the nuclear space accessible to them. Furthermore, translocations of PML-NBs relative to telomeres and their complexes with telomeres were evaluated. Based on these studies, a model is proposed in which the shortening of telomeres results in an increased mobility that could facilitate the formation of complexes between telomeres and PML-NBs.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据