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Heterochromatin Protein 1 Is Involved in Control of Telomere Elongation in Drosophila melanogaster

机译:异染色质蛋白1参与控制果蝇端粒的伸长。

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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.
机译:果蝇果蝇的端粒包含逆转录转座子样元件的阵列,它们分别是HeT-A和TART。它们转位至断裂的染色体末端与染色体修复和端粒延长有关。我们已经开发了一种遗传系统,能够确定端粒延伸事件的发生频率及其机制。不同基因型的品系之间的频率不同,表明有几个基因处于控制状态。在这里,我们显示涉及编码异染色质蛋白1(HP1)的 Su var 2 - 5 基因在调节端粒长度上。在杂合状态下不同的 Su var 2 - 5 突变会增加 HeT-断裂的染色体的 TART 附着终止了一百多次。附着通过 HeT-A / TART 转座或与其他端粒重组而发生。仅当DNA合成模板位于同一染色体而不是同源染色体上时, Su(var)2 - 5 突变才能大大提高基因转化的末端DNA延伸率。 。带有 Su(var)2 - 5 突变的果蝇系保持由 HeT-A 组成的极长的端粒和 TART 世代相传。因此,HP1在控制 D端粒伸长中起重要作用。黑色素瘤

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