Savitsky Mikhail, Kravchuk Oksana, Melnikova Larisa, Georgiev Pavel
Department of Control of Genetic Processes, Institute of Gene Biology, Russian Academy of Sciences, 117334 Moscow, Russia.
Mol Cell Biol. 2002 May;22(9):3204-18. doi: 10.1128/MCB.22.9.3204-3218.2002.
Telomeres of Drosophila melanogaster contain arrays of the retrotransposon-like elements HeT-A and TART. Their transposition to broken chromosome ends has been implicated in chromosome healing and telomere elongation. We have developed a genetic system which enables the determination of the frequency of telomere elongation events and their mechanism. The frequency differs among lines with different genotypes, suggesting that several genes are in control. Here we show that the Su(var)2-5 gene encoding heterochromatin protein 1 (HP1) is involved in regulation of telomere length. Different Su(var)2-5 mutations in the heterozygous state increase the frequency of HeT-A and TART attachment to the broken chromosome end by more than a hundred times. The attachment occurs through either HeT-A/TART transposition or recombination with other telomeres. Terminal DNA elongation by gene conversion is greatly enhanced by Su(var)2-5 mutations only if the template for DNA synthesis is on the same chromosome but not on the homologous chromosome. The Drosophila lines bearing the Su(var)2-5 mutations maintain extremely long telomeres consisting of HeT-A and TART for many generations. Thus, HP1 plays an important role in the control of telomere elongation in D. melanogaster.
黑腹果蝇的端粒包含逆转录转座子样元件HeT-A和TART的阵列。它们向断裂染色体末端的转座与染色体修复和端粒延长有关。我们开发了一种遗传系统,能够确定端粒延长事件的频率及其机制。频率在不同基因型的品系中有所不同,这表明有几个基因在起控制作用。在这里我们表明,编码异染色质蛋白1(HP1)的Su(var)2-5基因参与端粒长度的调控。杂合状态下不同的Su(var)2-5突变使HeT-A和TART附着到断裂染色体末端的频率增加了一百多倍。这种附着通过HeT-A/TART转座或与其他端粒的重组发生。只有当DNA合成的模板在同一条染色体上而不是在同源染色体上时,Su(var)2-5突变才会极大地增强通过基因转换进行的末端DNA延长。携带Su(var)2-5突变的果蝇品系会连续多代维持由HeT-A和TART组成的极长端粒。因此,HP1在黑腹果蝇端粒延长的控制中起着重要作用。