Scholarlink

<p>Proper oogenesis requires a programmed transition from an undifferentiated germ-cell gene expression program to a maternal gene-expression state. While this process depends on the heterochromatin-mediated silencing of germ-cell genes, the upstream mechanisms that enforce this transcriptional shift remain unclear. Here, we uncover a translation-driven chromatin remodeling program that promotes oocyte fate in Drosophila. Through a loss of function screen, we identify TORC1 activity (Mio, Raptor), ribosome biogenesis (Zfrp8, Bystin, Aramis), and a translation factor (eEF1α1) as essential for silencing the germ-cell program. We show that TORC1 activity increases during oocyte specification, and that disruption of TORC1 activity, translation, or ribosome biogenesis during this window impairs heterochromatin maintenance at germ-cell gene loci. Polysome profiling reveals that Zfrp8 promotes translation of the nuclear pore component Nucleoporin 44A (Nup44A), whose function is independently required for chromatin organization and repression of a cohort of germ-cell genes. Taken together, our findings reveal that a transient increase in translation orchestrates chromatin remodeling to ensure commitment to oocyte fate.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

TORC1-dependent translation drives chromatin remodeling during the germ-cell-to-maternal transition in Drosophila

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月26日

查看全文
  • Noor M Kotb,
  • Gulay Ulukaya,
  • Anupriya Ramamoorthy,
  • Lina Seojin Park,
  • Julia Tang,
  • Dan Hasson,
  • Prashanth Rangan

摘要

Proper oogenesis requires a programmed transition from an undifferentiated germ-cell gene expression program to a maternal gene-expression state. While this process depends on the heterochromatin-mediated silencing of germ-cell genes, the upstream mechanisms that enforce this transcriptional shift remain unclear. Here, we uncover a translation-driven chromatin remodeling program that promotes oocyte fate in Drosophila. Through a loss of function screen, we identify TORC1 activity (Mio, Raptor), ribosome biogenesis (Zfrp8, Bystin, Aramis), and a translation factor (eEF1α1) as essential for silencing the germ-cell program. We show that TORC1 activity increases during oocyte specification, and that disruption of TORC1 activity, translation, or ribosome biogenesis during this window impairs heterochromatin maintenance at germ-cell gene loci. Polysome profiling reveals that Zfrp8 promotes translation of the nuclear pore component Nucleoporin 44A (Nup44A), whose function is independently required for chromatin organization and repression of a cohort of germ-cell genes. Taken together, our findings reveal that a transient increase in translation orchestrates chromatin remodeling to ensure commitment to oocyte fate.