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Updated: Dec 27, 2025

Adult Mouse Digit Amputation and Regeneration: A Simple Model to Investigate Mammalian Blastema Formation and Intramembranous Ossification
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Epithelial Migration and Non-adhesive Periderm Are Required for Digit Separation during Mammalian Development.

Ghaidaa Kashgari1, Lina Meinecke2, William Gordon1

  • 1Department of Biological Chemistry, School of Medicine, University of California, Irvine, Irvine, CA, USA.

Developmental Cell
|February 29, 2020
PubMed
Summary

Syndactyly, or digit fusion, can result from mutations in Grainyhead like-3 (GRHL3). In Grhl3-deficient embryos, abnormal epidermal adhesion prevents digit separation, revealing new insights into limb development.

Keywords:
digit separationembryonic epidermisepithelial mechanismgrainyhead like-3interdigital cell deathlimb developmentperidermsyndactylyvan der Woude syndrome

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Area of Science:

  • Developmental Biology
  • Genetics
  • Molecular Biology

Background:

  • Syndactyly, the fusion of digits, is a congenital anomaly often associated with genetic syndromes like van der Woude syndrome.
  • Dominant-negative mutations in the epithelial transcription factor Grainyhead like-3 (GRHL3) cause a subset of van der Woude syndrome cases, leading to syndactyly in Grhl3-deficient mice.
  • While impaired interdigital cell death is a known cause of syndactyly, Grhl3-deficient embryos exhibit normal interdigital cell death, suggesting alternative mechanisms.

Purpose of the Study:

  • To investigate the underlying mechanisms of syndactyly in Grhl3-deficient embryos, focusing on epidermal developmental processes during digit separation.
  • To identify the specific role of GRHL3 in regulating epidermal behavior during limb development and digit morphogenesis.

Main Methods:

  • Analysis of Grhl3-deficient (Grhl3-/-) mouse embryos to examine interdigital tissue morphology and cell behavior.
  • Microscopic examination of epidermal development, including the formation and behavior of the interdigital epithelial tongue (IET).
  • Assessment of periderm adhesion properties and their role in digit separation.

Main Results:

  • Grhl3-/- embryos display normal migration of the interdigital epithelial tongue (IET) between digits.
  • However, the IET fails to bifurcate in Grhl3-/- embryos due to abnormal adhesion of the overlying periderm.
  • This abnormal epidermal adhesion, rather than impaired cell death, is identified as the primary cause of syndactyly in this model.

Conclusions:

  • The study identifies abnormal epidermal adhesion as a novel mechanism driving syndactyly in the absence of GRHL3 function.
  • Proper regulation of periderm adhesion by GRHL3 is crucial for the normal bifurcation of the interdigital epithelial tongue and subsequent digit separation.
  • These findings highlight the critical role of epidermal developmental processes in preventing congenital limb malformations like syndactyly.