首页    期刊浏览 2024年12月12日 星期四
登录注册

文章基本信息

  • 标题:p63 and Its Target Follistatin Maintain Salivary Gland Stem/Progenitor Cell Function through TGF-β/Activin Signaling
  • 本地全文:下载
  • 作者:Sangwon Min ; Akinsola Oyelakin ; Christian Gluck
  • 期刊名称:iScience
  • 印刷版ISSN:2589-0042
  • 出版年度:2020
  • 卷号:23
  • 期号:9
  • 页码:1-44
  • DOI:10.1016/j.isci.2020.101524
  • 语种:English
  • 出版社:Elsevier
  • 摘要:SummaryMultipotent ΔNp63-positive cells maintain all epithelial cell lineages of the embryonic and adult salivary gland (SG). However, the molecular mechanisms by which ΔNp63 regulates stem/progenitor (SP) cell populations in the SG remains elusive. To understand the role of ΔNp63 in directing cell fate choices in this gland, we have generated ΔNp63-deleted adult mice and primary salivary cell cultures to probe alterations in SP cell differentiation and function. In parallel, we have leveraged RNA-seq and ChIP-seq-based characterization of the ΔNp63-driven cistrome and scRNA-seq analysis to molecularly interrogate altered SG cellular identities and differentiation states dependent on ΔNp63. Our studies reveal that ablation of ΔNp63 results in a loss of the SP cell population and skewed differentiation that is mediated by Follistatin-dependent dysregulated TGF-β/Activin signaling. These findings offer new revelations into the SP cell gene regulatory networks that are likely to be relevant for normal or diseased SG states.Graphical AbstractDisplay OmittedHighlights•Loss of ΔNp63 expression results in a block in salivary gland cell differentiation•p63 maintains salivary gland stem and progenitor cell proliferation•p63 acts upstream of TGF-β/Activin signaling by directly regulatingFstexpressionCell Biology; Developmental Biology; Stem Cells Research
国家哲学社会科学文献中心版权所有