Telomere elongation is under the control of the RNAi-based mechanism in the Drosophila germline

Telomere elongation is under the control of the RNAi-based mechanism in the Drosophila germline
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DOI:
10.1101/gad.370206
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发表时间:
2006-02-01
影响因子:
10.5
通讯作者:
Gvozdev, V
Gvozdev, V
中科院分区:
生物学1区
文献类型:
--
作者:
Savitsky, M;Kwon, D;Gvozdev, V

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在果蝇中,端粒是通过专门的端粒逆转录元件HeT-A、TAHRE和TART的转座来维持的,而不是在其他真核生物中由端粒酶产生的短DNA重复序列。在这里,我们牵连的RNA干扰机制在控制果蝇的卵巢端粒长度。端粒逆转录因子转录本的丰度由于sture-E和aub基因的突变而上调,所述基因分别编码Argonaute家族的推定的RNA解旋酶和蛋白质,其与RNA干扰(RNAi)机制相关。这些突变导致端粒元件反转录转座到断裂的染色体末端的频率增加。sture-E突变消除了卵巢中的HeT-A和TART短RNA,这表明在果蝇种系中控制端粒维持的基于RNAi的机制。在携带一个剂量的突变sture-E或aub等位基因的个体中,TART而不是HeT-A附着的频率增加表明TART是RNAi机制的主要靶标。与此同时,我们检测到增强HeT-A附着到纯合sture-E突变体的卵母细胞中断裂的染色体末端。双链RNA(dsRNA)介导的端粒逆转录元件转位的控制可能发生在减数分裂前阶段,导致配子前体中适当的端粒长度的维持。
Telomeres in Drosophila are maintained by transposition of specialized telomeric retroelements HeT-A, TAHRE, and TART instead of the short DNA repeats generated by telomerase in other eukaryotes. Here we implicate the RNA interference machinery in the control of Drosophila telomere length in ovaries. The abundance of telomeric retroelement transcripts is up-regulated owing to mutations in the spn-E and aub genes, encoding a putative RNA helicase and protein of the Argonaute family, respectively, which are related to the RNA interference (RNAi) machinery. These mutations cause an increase in the frequency of telomeric element retrotransposition to a broken chromosome end. spn-E mutations eliminate HeT-A and TART short RNAs in ovaries, suggesting an RNAi-based mechanism in the control of telomere maintenance in the Drosophila germline. Enhanced frequency of TART, but not HeT-A, attachments in individuals carrying one dose of mutant spn-E or aub alleles suggests that TART is a primary target of the RNAi machinery. At the same time, we detected enhanced HeT-A attachments to broken chromosome ends in oocytes from homozygous spn-E mutants. Double-stranded RNA (dsRNA)-mediated control of telomeric retroelement transposition may occur at premeiotic stages, resulting in the maintenance of appropriate telomere length in gamete precursors.