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<p>The pluripotency state of embryonic stem cells (ESCs) is determined by both their epigenome and transcriptome. Sgf29, a subunit of the transcriptional co-activator complex SAGA, plays a critical role in a wide range of biological processes. However, whether and how Sgf29 mediates epigenetic modifications and pluripotency gene transcription is not fully understood. Herein, we found that <i>Sgf29</i> knockout (KO) induced the differentiation of mouse ESCs (mESCs) by reducing H3K9ac and chromatin accessibility at the promoters and enhancers of key pluripotency genes. Interestingly, Sgf29 interacted with Oct4 and Nanog, but not Sox2, to co-regulate pluripotency genes. <i>Sgf29</i> KO reduced the binding of Oct4 to the promoter and enhancer loci of <i>Nanog</i> and <i>Klf4</i>, leading to reduced expression of themselves and their downstream pluripotency-related genes. Furthermore, <i>Sgf29</i> knockdown (KD) significantly reduced blastocyst rate and decreased H3K9ac at the blastocyst stage, leading to aberrant Oct4 and Nanog in the pre-implantation embryo. Together, these findings suggest that Sgf29 maintains chromatin accessibility and regulates the transcription of pluripotency-related genes by forming a functional complex with Oct4 and Nanog, playing a critical role in the regulation of pluripotent cell fate.</p>

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Sgf29 regulates pluripotency by maintaining chromatin accessibility and promoting the expression of core transcription factors

  • 期刊论文

  • 发表日期：

    2026年3月13日

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  • Yanling Qiu,
  • Sisi Yin,
  • Tianqi Cao,
  • Tengteng Xu,
  • Simiao Liu,
  • Zihui Luo,
  • Yitong Zhou,
  • Haiying Liu,
  • Junjiu Huang

摘要

The pluripotency state of embryonic stem cells (ESCs) is determined by both their epigenome and transcriptome. Sgf29, a subunit of the transcriptional co-activator complex SAGA, plays a critical role in a wide range of biological processes. However, whether and how Sgf29 mediates epigenetic modifications and pluripotency gene transcription is not fully understood. Herein, we found that Sgf29 knockout (KO) induced the differentiation of mouse ESCs (mESCs) by reducing H3K9ac and chromatin accessibility at the promoters and enhancers of key pluripotency genes. Interestingly, Sgf29 interacted with Oct4 and Nanog, but not Sox2, to co-regulate pluripotency genes. Sgf29 KO reduced the binding of Oct4 to the promoter and enhancer loci of Nanog and Klf4, leading to reduced expression of themselves and their downstream pluripotency-related genes. Furthermore, Sgf29 knockdown (KD) significantly reduced blastocyst rate and decreased H3K9ac at the blastocyst stage, leading to aberrant Oct4 and Nanog in the pre-implantation embryo. Together, these findings suggest that Sgf29 maintains chromatin accessibility and regulates the transcription of pluripotency-related genes by forming a functional complex with Oct4 and Nanog, playing a critical role in the regulation of pluripotent cell fate.