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端粒逆转录转座子与细胞周期的转录偶联

Transcriptional coupling of telomeric retrotransposons with the cell cycle.

作者信息

Liu Mengmeng, Xie Xiao-Jun, Li Xiao, Ren Xingjie, Sun Jasmine L, Lin Zhen, Hemba-Waduge Rajitha-Udakara-Sampath, Ji Jun-Yuan

机构信息

Department of Biochemistry and Molecular Biology, Tulane University School of Medicine, Louisiana Cancer Research Center, 1700 Tulane Avenue, New Orleans, LA 70112, USA.

Department of Molecular and Cellular Medicine, College of Medicine, Texas A&M University Health Science Center, College Station, TX 77843, USA.

出版信息

Sci Adv. 2025 Jan 3;11(1):eadr2299. doi: 10.1126/sciadv.adr2299.

DOI:10.1126/sciadv.adr2299
PMID:39752503
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11698117/
Abstract

Unlike most species that use telomerase for telomere maintenance, many dipterans, including , rely on three telomere-specific retrotransposons (TRs)-, , and -to form tandem repeats at chromosome ends. Although TR transcription is crucial in their life cycle, its regulation remains poorly understood. This study identifies the Mediator complex, E2F1-Dp, and Scalloped/dTEAD as key regulators of TR transcription. Reducing the activity of the Mediator or Sd/dTEAD increases TR expression and telomere length, while overexpressing E2F1-Dp or depleting Rbf1 stimulates TR transcription. The Mediator and Sd/dTEAD regulate this process through E2F1-Dp. CUT&RUN (Cleavage under targets and release using nuclease) analysis shows direct binding of CDK8, Dp, and Sd/dTEAD to telomeric repeats, with motif enrichment revealing E2F- and TEAD-binding sites. These findings uncover the Mediator complex's role in controlling TR transcription and telomere length through E2F1-Dp and Sd, coupling the transcriptional regulation of the TR life cycle with host cell-cycle machinery to protect chromosome ends in .

摘要

与大多数利用端粒酶维持端粒的物种不同，许多双翅目昆虫，包括[具体物种未给出]，依赖三种端粒特异性逆转座子（TRs）——[TRs名称未给出]、[TRs名称未给出]和[TRs名称未给出]——在染色体末端形成串联重复序列。尽管TR转录在它们的生命周期中至关重要，但其调控机制仍知之甚少。本研究确定中介体复合物、E2F1-Dp和扇贝状蛋白/果蝇TEAD为TR转录的关键调节因子。降低中介体或扇贝状蛋白/果蝇TEAD的活性会增加TR表达和端粒长度，而过表达E2F1-Dp或耗尽Rbf1则会刺激TR转录。中介体和扇贝状蛋白/果蝇TEAD通过E2F1-Dp调节这一过程。CUT&RUN（靶向切割并使用核酸酶释放）分析表明CDK8、Dp和扇贝状蛋白/果蝇TEAD直接结合到端粒重复序列上，基序富集揭示了E2F和TEAD结合位点。这些发现揭示了中介体复合物通过E2F1-Dp和扇贝状蛋白在控制TR转录和端粒长度中的作用，将TR生命周期的转录调控与宿主细胞周期机制耦合起来，以保护[具体物种未给出]的染色体末端。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f90/11698117/308a3ecb3f81/sciadv.adr2299-f7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f90/11698117/308a3ecb3f81/sciadv.adr2299-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f90/11698117/5962eabc9ca4/sciadv.adr2299-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f90/11698117/6ecb5603ef75/sciadv.adr2299-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f90/11698117/a09dd48cfa5b/sciadv.adr2299-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f90/11698117/193e8b700dd3/sciadv.adr2299-f4.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f90/11698117/308a3ecb3f81/sciadv.adr2299-f7.jpg

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