De Lange T, Kooter J M, Michels P A, Borst P
Nucleic Acids Res. 1983 Dec 10;11(23):8149-65. doi: 10.1093/nar/11.23.8149.
Activation of the gene coding for variant surface glycoprotein (VSG) 118 in Trypanosoma brucei proceeds via a duplicative transposition to a telomeric expression site. The resulting active expression-linked extra copy (ELC) is usually flanked by DNA that lacks sites for most restriction enzymes and that is thought to interfere with the cloning of the ELC as recombinant DNA in Escherichia coli. We have circumvented this problem by cloning an aberrant 118 ELC gene, flanked at the 3'-side by at least 1 kb DNA, that contains restriction enzyme sites. Our analysis shows that this DNA and the 3'-end of the 118 ELC gene are derived from another VSG gene (1.1006) that is permanently located at a telomeric position. We propose that the 3'-end of the 1.1006 gene and (all of) its 3' flanking sequence moved to the expression site by a telomere conversion. Such a telomere conversion can also account for the appearance of an extra copy of the 1.1006 gene detected in a sub-population of our trypanosome strain.
布氏锥虫中编码变异表面糖蛋白（VSG）118的基因激活是通过重复转座至端粒表达位点来进行的。由此产生的与表达相关的活性额外拷贝（ELC）通常两侧是缺乏大多数限制酶切割位点的DNA，人们认为这种DNA会干扰ELC作为重组DNA在大肠杆菌中的克隆。我们通过克隆一个异常的118 ELC基因解决了这个问题，该基因在3'端侧翼至少有1 kb的DNA，其中包含限制酶切割位点。我们的分析表明，这段DNA和118 ELC基因的3'端源自另一个永久位于端粒位置的VSG基因（1.1006）。我们提出，1.1006基因的3'端及其（全部）3'侧翼序列通过端粒转换转移到了表达位点。这样的端粒转换也可以解释在我们的锥虫菌株亚群中检测到的1.1006基因额外拷贝的出现。
