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Periderm: Life-cycle and function during orofacial and epidermal development.

Nigel L Hammond1, Jill Dixon1, Michael J Dixon1

  • 1Faculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, Michael Smith Building, University of Manchester, Oxford Road, Manchester, M13 9PT, United Kingdom.

Seminars in Cell & Developmental Biology
|August 15, 2017
PubMed
Summary
This summary is machine-generated.

The embryonic periderm prevents abnormal tissue fusions during palate development. Disruptions in periderm function lead to congenital conditions like cleft palate and popliteal pterygium syndrome.

Keywords:
Cleft palateEctodermPalatal fusionPeridermPterygium syndromes

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Area of Science:

  • Developmental Biology
  • Embryogenesis
  • Craniofacial Development

Background:

  • Secondary palate formation is a complex embryonic process prone to disruption, leading to cleft palate.
  • Pathological fusion between developing palatal shelves and mandibular/lingual epithelia must be prevented.
  • The periderm, a transient embryonic epithelial layer, plays a crucial role in mediating these interactions.

Purpose of the Study:

  • To elucidate the role of the embryonic periderm in preventing pathological adhesions during secondary palate development.
  • To understand the molecular mechanisms underlying periderm formation and its regulation.
  • To investigate the link between periderm dysfunction and congenital adhesion syndromes.

Main Methods:

  • Analysis of periderm formation patterns and adhesion complex expression during embryogenesis.
  • Genetic studies of congenital syndromes associated with periderm defects (e.g., popliteal pterygium syndrome).
  • Investigating the role of transcription factors (e.g., p63) and signaling pathways (e.g., TGFβ3) in periderm function and midline fusion.

Main Results:

  • The periderm forms early, exhibits polarized adhesion, and is shed as the epidermis matures.
  • Disruptions in periderm formation underlie syndromes with multiple inter-epithelial adhesions.
  • TGFβ3-mediated p63 downregulation in medial edge epithelia is critical for palate fusion by allowing periderm migration and reducing midline proliferation.

Conclusions:

  • The periderm is essential for preventing pathological adhesions between apposed epithelia during embryogenesis.
  • Periderm dysfunction is implicated in various congenital birth defects.
  • Precise regulation of periderm function and its interaction with underlying epithelia is vital for normal secondary palate development and fusion.