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逆转座子3S18形成自我保护聚集体并延长卵子发生中期。

Retrotransposon 3S18 forms self-protective aggregates and prolongs mid-oogenesis.

作者信息

Shen Dan, Xu Yaqian, Shi Qi, Li Chongyang, Meng Zhe, Wen Qiuju, Wang Chenhui, Dou Kun

机构信息

School of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China.

School of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China.

出版信息

Cell Rep. 2025 Jul 22;44(7):115914. doi: 10.1016/j.celrep.2025.115914. Epub 2025 Jun 24.

DOI:10.1016/j.celrep.2025.115914
PMID:40560732
Abstract

Transposons are prevalent across nearly all species due to their capacity to mobilize in the host genome. However, their products may begin to affect the host before integration occurs. Here, we identified that the activation of transposons results in significantly smaller mid-stage oocytes and prolonged mid-oogenesis of Drosophila. Notably, one specific long terminal repeat (LTR) retrotransposon, 3S18, primarily contributes to this phenotype. We found that 3S18 mRNA and its integrase form micrometer-scaled ribonucleoprotein aggregates at cell-cell bridges during these stages. Interestingly, mutants that suppress the formation of these RNP aggregates substantially reduce 3S18 mRNA levels, suggesting that 3S18 aggregates serve functional importance in protecting the retrotransposon products. Live imaging reveals that the accumulation of 3S18 RNP aggregates obstructs host material transportation, resulting in prolonged mid-oogenesis. Finally, forcefully extending oogenesis significantly enhances 3S18 propagation. Our study highlights the unique characteristics of 3S18 and its impact on host development. It may shed light on studies of other parasitic elements, including viruses.

摘要

转座子因其能够在宿主基因组中移动而在几乎所有物种中普遍存在。然而,它们的产物可能在整合发生之前就开始影响宿主。在这里,我们发现转座子的激活会导致果蝇中期卵母细胞显著变小,以及中期卵子发生延长。值得注意的是,一种特定的长末端重复(LTR)逆转录转座子3S18主要导致了这种表型。我们发现,在这些阶段,3S18 mRNA及其整合酶在细胞间桥处形成微米级的核糖核蛋白聚集体。有趣的是,抑制这些核糖核蛋白聚集体形成的突变体显著降低了3S18 mRNA水平,这表明3S18聚集体在保护逆转录转座子产物方面具有重要功能。实时成像显示,3S18核糖核蛋白聚集体的积累阻碍了宿主物质运输,导致中期卵子发生延长。最后,强行延长卵子发生显著增强了3S18的传播。我们的研究突出了3S18的独特特征及其对宿主发育的影响。它可能为包括病毒在内的其他寄生元件的研究提供启示。

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