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<p>PTEN-induced kinase 1 (<i>Pink1</i>), a familial Parkinson’s associated gene, is a key regulator of mitochondrial and cellular energy homeostasis. Mutations in <i>Pink1</i> disrupt mitophagy and perturbations in gastrointestinal homeostasis. This suggests the possibility that <i>Pink1</i> deficiency may influence neurodegenerative processes by altering gut-to-brain signaling mechanisms. To facilitate investigation of gut-specific consequences of <i>Pink1</i> deficiency, we generated a single-nucleus RNA sequencing (snRNA-seq) dataset from gut tissue of wild-type (WT) and <i>Pink1</i> knockout (KO) mice. We identified major cell populations such as goblet cells, immune cells, and colonocytes, and characterized their transcriptional profiles. For technical validation, we utilized a publicly available murine gut (snRNA-seq) dataset. We then applied anchor-based label transfer and confirmed cell-type assignments via random forest classification. This rigorously validated dataset provides a robust resource for exploring shifts in cell-type composition and transcriptional alterations associated with <i>Pink1</i> loss.</p>

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A single-nucleus RNA-seq dataset of the colon in Pink1-deficient and wild-type mice

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月6日

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  • Muhammad Junaid,
  • Soo Jung Park,
  • Yiseul Bae,
  • Eun Jeong Lee,
  • Su Bin Lim

摘要

PTEN-induced kinase 1 (Pink1), a familial Parkinson’s associated gene, is a key regulator of mitochondrial and cellular energy homeostasis. Mutations in Pink1 disrupt mitophagy and perturbations in gastrointestinal homeostasis. This suggests the possibility that Pink1 deficiency may influence neurodegenerative processes by altering gut-to-brain signaling mechanisms. To facilitate investigation of gut-specific consequences of Pink1 deficiency, we generated a single-nucleus RNA sequencing (snRNA-seq) dataset from gut tissue of wild-type (WT) and Pink1 knockout (KO) mice. We identified major cell populations such as goblet cells, immune cells, and colonocytes, and characterized their transcriptional profiles. For technical validation, we utilized a publicly available murine gut (snRNA-seq) dataset. We then applied anchor-based label transfer and confirmed cell-type assignments via random forest classification. This rigorously validated dataset provides a robust resource for exploring shifts in cell-type composition and transcriptional alterations associated with Pink1 loss.