Ancelin K, Brun C, Gilson E
Laboratoire de Biologie Moléculaire et Cellulaire, Ecole Normale Supérieure de Lyon, UMR49 CNRS/ENS, France.
Bioessays. 1998 Nov;20(11):879-83. doi: 10.1002/(SICI)1521-1878(199811)20:11<879::AID-BIES2>3.0.CO;2-I.
A major issue in telomere research is to understand how the integrity of chromosome ends is preserved. A recent study shows that expression of a dominant-negative form of the human telomeric protein TRF2 increases the number of chromosome fusions in immortalized cells and decreases the quantity of G-rich telomeric DNA 3' overhang, the G tail. Consequently, TRF2 appears to control the structure of the very end of the chromosomal DNA molecule and to prevent recombination between two telomeres. Remarkably, the same study reveals a potential role of TRF2 in cell division control.
端粒研究中的一个主要问题是了解染色体末端的完整性是如何得以维持的。最近一项研究表明，人类端粒蛋白TRF2的显性负性形式的表达增加了永生化细胞中染色体融合的数量，并减少了富含G的端粒DNA 3' 突出端（即G尾）的数量。因此，TRF2似乎控制着染色体DNA分子最末端的结构，并防止两个端粒之间发生重组。值得注意的是，同一研究揭示了TRF2在细胞分裂控制中的潜在作用。
