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SSUP-72/PINN-1协调秀丽隐杆线虫中RNA聚合酶II的3'端暂停和发育基因表达。

SSUP-72/PINN-1 coordinates RNA-polymerase II 3' pausing and developmental gene expression in C. elegans.

作者信息

Stubbe François-Xavier, Ponsard Pauline, Steiner Florian A, Hermand Damien

机构信息

URPHYM-GEMO, The University of Namur, Namur, Belgium.

Department of Molecular and Cellular Biology, Faculty of Sciences, University of Geneva, Geneva, Switzerland.

出版信息

Nat Commun. 2025 Mar 17;16(1):2624. doi: 10.1038/s41467-025-57847-x.

DOI:10.1038/s41467-025-57847-x
PMID:40097442
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11914089/
Abstract

During exit from Caenorhabditis elegans (C. elegans) L1 developmental arrest, a network of growth- and developmental genes is activated, many of which are organized into operons where transcriptional termination is uncoupled from mRNA 3'-end processing. CDK-12-mediated Pol II CTD S2 phosphorylation enhances SL2 trans-splicing at downstream operonic genes, preventing premature termination and ensuring proper gene expression for developmental progression. Using a genetic screen, we identified the SSUP-72/PINN-1 module as a suppressor of defects induced by CDK-12 inhibition. Loss of SSUP-72/PINN-1 bypasses the requirement for CDK-12 in post-embryonic development. Genome-wide analyses reveal that SSUP-72, a CTD S5P phosphatase, affects Pol II 3' pausing and regulates intra-operon termination. Our findings establish SSUP-72/PINN-1 as a key regulator of Pol II dynamics, coordinating operonic gene expression and growth during C. elegans post-embryonic development.

摘要

在秀丽隐杆线虫（C. elegans）从L1发育停滞状态退出的过程中，一个由生长和发育基因组成的网络被激活，其中许多基因被组织成操纵子，转录终止与mRNA 3'端加工解偶联。CDK-12介导的Pol II CTD S2磷酸化增强了下游操纵子基因处的SL2反式剪接，防止过早终止并确保发育进程中基因的正确表达。通过遗传筛选，我们鉴定出SSUP-72/PINN-1模块是CDK-12抑制诱导缺陷的抑制因子。SSUP-72/PINN-1的缺失绕过了胚胎后发育中对CDK-12的需求。全基因组分析表明，CTD S5P磷酸酶SSUP-72影响Pol II 3'停顿并调节操纵子内终止。我们的研究结果确立了SSUP-72/PINN-1作为Pol II动力学的关键调节因子，在秀丽隐杆线虫胚胎后发育过程中协调操纵子基因表达和生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5cf/11914089/9d7258e798bb/41467_2025_57847_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5cf/11914089/048c67aaf82a/41467_2025_57847_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5cf/11914089/90cc4b2f7b32/41467_2025_57847_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5cf/11914089/d24bf172ae11/41467_2025_57847_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5cf/11914089/9d7258e798bb/41467_2025_57847_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5cf/11914089/048c67aaf82a/41467_2025_57847_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5cf/11914089/90cc4b2f7b32/41467_2025_57847_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5cf/11914089/d24bf172ae11/41467_2025_57847_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5cf/11914089/9d7258e798bb/41467_2025_57847_Fig4_HTML.jpg

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