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<p>Cranial sutures are essential for skull growth and tissue homeostasis. Among them, the coronal suture is most frequently affected in syndromic craniosynostosis, yet the mechanisms underlying this preferential involvement remain unclear. Here, we show that the coronal suture mesenchyme undergoes a postnatal lineage transition from mesodermal to cranial neural crest origin, facilitated by dural cell migration into the suture. Mechanistically, this migration is regulated by suture TGFβ signals to <i>Tgfbr2+</i> dural cells. Loss of dural <i>Tgfbr2</i> impairs this cell migration into the suture, reduces the <i>Gli1</i>+ suture progenitor pool, and causes premature coronal suture fusion. Furthermore, in <i>Twist1</i><sup><i>+/-</i></sup> mice recapitulating human Saethre-Chotzen syndrome, upregulated decorin leads to compromised TGFβ signaling, which impairs dural cell migration, leading to craniosynostosis. Significantly, restoring TGFβ signaling rescues coronal suture patency in <i>Twist1</i><sup><i>+/-</i></sup> mice. These findings identify the critical role of TGFβ-mediated dural-suture interactions, particularly dural cell migration, in maintaining coronal suture patency and provide an explanation for the preferential coronal fusion in syndromic craniosynostosis.</p>

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TGFβ-mediated dural progenitor cell migration into the coronal suture is crucial for preventing craniosynostosis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月19日

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  • Peng Chen,
  • Lin Meng,
  • Lin Lan,
  • Jifan Feng,
  • Tingwei Guo,
  • Lu Gao,
  • Hana Hekmat,
  • Calista Ly,
  • Mingyi Zhang,
  • Sa Cha,
  • Thach-Vu Ho,
  • Yang Chai

摘要

Cranial sutures are essential for skull growth and tissue homeostasis. Among them, the coronal suture is most frequently affected in syndromic craniosynostosis, yet the mechanisms underlying this preferential involvement remain unclear. Here, we show that the coronal suture mesenchyme undergoes a postnatal lineage transition from mesodermal to cranial neural crest origin, facilitated by dural cell migration into the suture. Mechanistically, this migration is regulated by suture TGFβ signals to Tgfbr2+ dural cells. Loss of dural Tgfbr2 impairs this cell migration into the suture, reduces the Gli1+ suture progenitor pool, and causes premature coronal suture fusion. Furthermore, in Twist1+/- mice recapitulating human Saethre-Chotzen syndrome, upregulated decorin leads to compromised TGFβ signaling, which impairs dural cell migration, leading to craniosynostosis. Significantly, restoring TGFβ signaling rescues coronal suture patency in Twist1+/- mice. These findings identify the critical role of TGFβ-mediated dural-suture interactions, particularly dural cell migration, in maintaining coronal suture patency and provide an explanation for the preferential coronal fusion in syndromic craniosynostosis.