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piRNA 缺失的小鼠精母细胞细胞质中的反转录转座子 LINE-1 体：核糖核蛋白克服整合应激反应。

Retrotransposon LINE-1 bodies in the cytoplasm of piRNA-deficient mouse spermatocytes: Ribonucleoproteins overcoming the integrated stress response.

机构信息

Department of Embryology, Carnegie Institution for Science, Baltimore, Maryland, United States of America.

The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.

出版信息

PLoS Genet. 2023 Jun 12;19(6):e1010797. doi: 10.1371/journal.pgen.1010797. eCollection 2023 Jun.

DOI:10.1371/journal.pgen.1010797
PMID:37307272
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10289378/
Abstract

Transposable elements (TE) are mobile DNA sequences whose excessive proliferation endangers the host. Although animals have evolved robust TE-targeting defenses, including Piwi-interacting (pi)RNAs, retrotransposon LINE-1 (L1) still thrives in humans and mice. To gain insights into L1 endurance, we characterized L1 Bodies (LBs) and ORF1p complexes in germ cells of piRNA-deficient Maelstrom null mice. We report that ORF1p interacts with TE RNAs, genic mRNAs, and stress granule proteins, consistent with earlier studies. We also show that ORF1p associates with the CCR4-NOT deadenylation complex and PRKRA, a Protein Kinase R factor. Despite ORF1p interactions with these negative regulators of RNA expression, the stability and translation of LB-localized mRNAs remain unchanged. To scrutinize these findings, we studied the effects of PRKRA on L1 in cultured cells and showed that it elevates ORF1p levels and L1 retrotransposition. These results suggest that ORF1p-driven condensates promote L1 propagation, without affecting the metabolism of endogenous RNAs.

摘要

转座元件 (TE) 是可移动的 DNA 序列，其过度增殖会危及宿主。尽管动物已经进化出强大的 TE 靶向防御机制，包括 Piwi 相互作用 (pi)RNAs，但 LINE-1 反转录转座子 (L1) 在人类和小鼠中仍然大量存在。为了深入了解 L1 的持续存在，我们在 piRNA 缺失的 Maerlstrom 缺失小鼠的生殖细胞中对 L1 体 (LB) 和 ORF1p 复合物进行了表征。我们报告说，ORF1p 与 TE RNA、基因 mRNA 和应激颗粒蛋白相互作用，与早期研究一致。我们还表明，ORF1p 与 CCR4-NOT 脱腺苷酸化复合物和 PRKRA（蛋白激酶 R 因子）相关。尽管 ORF1p 与这些 RNA 表达的负调控因子相互作用，但 LB 定位的 mRNA 的稳定性和翻译保持不变。为了仔细研究这些发现，我们研究了 PRKRA 对培养细胞中 L1 的影响，并表明它会提高 ORF1p 水平和 L1 反转录转座。这些结果表明，ORF1p 驱动的凝聚物促进了 L1 的传播，而不会影响内源性 RNA 的代谢。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/9fc78174834b/pgen.1010797.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/b7fb63d60b0b/pgen.1010797.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/83aef71b60d0/pgen.1010797.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/163e9962032c/pgen.1010797.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/61b38db7ec13/pgen.1010797.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/1cffec7830e2/pgen.1010797.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/29005195aef6/pgen.1010797.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/9fc78174834b/pgen.1010797.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/b7fb63d60b0b/pgen.1010797.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/83aef71b60d0/pgen.1010797.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/163e9962032c/pgen.1010797.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/61b38db7ec13/pgen.1010797.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/1cffec7830e2/pgen.1010797.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/29005195aef6/pgen.1010797.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f01/10289378/9fc78174834b/pgen.1010797.g007.jpg

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