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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >UBR2 mediates transcriptional silencing during spermatogenesis via histone ubiquitination
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UBR2 mediates transcriptional silencing during spermatogenesis via histone ubiquitination

机译：UBR2通过组蛋白泛素介导精子发生过程中的转录沉默

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摘要

Ubiquitination of histones provides an important mechanism regulating chromatin remodeling and gene expression. Recent studies have revealed ubiquitin ligases involved in histone ubiquitination, yet the responsible enzymes and the function of histone ubiquitination in spermatogenesis remain unclear. We have previously shown that mice lacking the ubiquitin ligase UBR2, one of the recognition E3 components of the N-end rule proteolytic pathway, are infertile associated with meiotic arrest at prophase I. We here show that UBR2 localizes to meiotic chromatin regions, including unsynapsed axial elements linked to chromatin inactivation, and mediates transcriptional silencing via the ubiquitination of histone H2A. UBR2 interacts with the ubiquitin conjugating enzyme HR6B and its substrate H2A and promotes the HR6B-H2A interaction and the HR6B-to-H2A transfer of ubiquitin. UBR2 and ubiquitinated H2A (uH2A) spatiotemporally mark meiotic chromatin regions subject to transcriptional silencing, and UBR2-deficient spermatocytes fail to induce the ubiquitination of H2A during meiosis. UBR2-deficient spermatocytes are profoundly impaired in chromosome-wide transcriptional silencing of genes linked to unsynapsed axes of the X and Y chromosomes. Our findings suggest that insufficiency in UBR2-dependent histone ubiquitination triggers a pachytene checkpoint system, providing a new insight into chromatin remodeling and gene expression regulation.
机译：组蛋白的泛素化提供了调节染色质重塑和基因表达的重要机制。最近的研究表明泛素连接酶参与组蛋白泛素化，但尚不清楚负责的酶和组蛋白泛素化在精子发生中的功能。我们以前已经表明，缺乏泛素连接酶UBR2（N端规则蛋白水解途径的识别E3成分之一）的小鼠在前期I时与减数分裂停滞有关。轴向元件与染色质失活有关，并通过组蛋白H2A的泛素化介导转录沉默。 UBR2与泛素结合酶HR6B及其底物H2A相互作用，并促进泛素的HR6B-H2A相互作用和HR6B向H2A的转移。 UBR2和泛素化的H2A（uH2A）时空标记减数分裂染色质区域，使其受到转录沉默，而UBR2缺失的精母细胞在减数分裂期间无法诱导H2A泛素化。 UBR2缺陷的精母细胞在与X和Y染色体未突触轴相关的基因的全染色体转录沉默中受到严重损害。我们的发现表明，UBR2依赖性组蛋白泛素化不足会触发粗线检查点系统，从而为染色质重塑和基因表达调控提供新的见解。

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  • 作者

    Jee Young An; Eun-A. Kim; Yonghua Jiang; Adriana Zakrzewska; Dong Eun Kim; Min Jae Lee; Inhee Mook-Jung; Yi Zhang; Yong Tae Kwon;

  • 作者单位

    Center for Pharmacogenetics and Department of Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, Pittsburgh, PA 15261;

    rnCenter for Pharmacogenetics and Department of Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, Pittsburgh, PA 15261;

    rnCenter for Pharmacogenetics and Department of Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, Pittsburgh, PA 15261;

    rnCenter for Pharmacogenetics and Department of Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, Pittsburgh, PA 15261;

    rnCenter for Pharmacogenetics and Department of Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, Pittsburgh, PA 15261;

    rnDepartment of Cell Biology, Harvard Medical School, Boston, MA 02115;

    rnDepartment of Biochemistry and Biomedical Science, Seoul National University College of Medicine, Seoul 110-799, Korea;

    rnDepartment of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599;

    rnCenter for Pharmacogenetics and Department of Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, Pittsburgh, PA 15261;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    chromatin inactivation; H2A; meiosis; N-end rule; ubiquitin;

    机译：染色质失活;H2A;减数分裂N端规则;泛素;

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