Scholarlink

<p>The vertebrate retina serves as a model for studying neurogenesis and cell fate specification, with retinal progenitor cells following a tightly regulated temporal sequence to generate distinct cell types. Meis1 and Meis2 are transcription factors implicated in early retinal development, but their role in late-stage RPCs remains poorly understood. Here, we investigate whether <i>Meis1</i> and <i>Meis2</i> overexpression in postnatal mouse RPCs can alter temporal identity and induce early-born cell types. Using electroporation and single-cell RNA sequencing, we find that while these factors modestly upregulate early-stage gene regulatory network components, they do not repress late-stage transcription factors or induce early-born retinal cells. <i>Meis1</i> overexpression reduces proliferation and inhibits neurogenesis, whereas <i>Meis2</i> overexpression accelerates neurogenic progression without altering fate commitment. Our findings suggest that overexpression of <i>Meis1</i> and <i>Meis2</i> modulate largely non-overlapping aspects of temporal identity and neurogenic competence but are insufficient to fully reprogram late-stage progenitors. These results have implications for regenerative strategies aimed at reprogramming retinal cells for therapeutic purposes.</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

Overexpression of Meis factors in late-stage retinal progenitors yields complex effects on temporal patterning and neurogenesis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月3日

查看全文
  • Patrick Leavey,
  • Lizhi Jiang,
  • Nicole Pannullo,
  • Clayton Santiago,
  • Seth Blackshaw

摘要

The vertebrate retina serves as a model for studying neurogenesis and cell fate specification, with retinal progenitor cells following a tightly regulated temporal sequence to generate distinct cell types. Meis1 and Meis2 are transcription factors implicated in early retinal development, but their role in late-stage RPCs remains poorly understood. Here, we investigate whether Meis1 and Meis2 overexpression in postnatal mouse RPCs can alter temporal identity and induce early-born cell types. Using electroporation and single-cell RNA sequencing, we find that while these factors modestly upregulate early-stage gene regulatory network components, they do not repress late-stage transcription factors or induce early-born retinal cells. Meis1 overexpression reduces proliferation and inhibits neurogenesis, whereas Meis2 overexpression accelerates neurogenic progression without altering fate commitment. Our findings suggest that overexpression of Meis1 and Meis2 modulate largely non-overlapping aspects of temporal identity and neurogenic competence but are insufficient to fully reprogram late-stage progenitors. These results have implications for regenerative strategies aimed at reprogramming retinal cells for therapeutic purposes.