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MLL4 regulates postnatal palate growth and midpalatal suture development
Jung-Mi Lee1, Hunmin Jung1, Bruno de Paula Machado Pasqua1
1Department of Oral Biology, School of Dental Medicine, University at Buffalo, The State University of New York, Buffalo, NY 14214, U.S.A.
Biorxiv : the Preprint Server for Biology
|October 7, 2024
Summary
MLL4 (KMT2D) is crucial for palate development. Its absence in mice causes midfacial defects and growth deficits by impairing midpalatal suture cartilage development.
Area of Science:
- Developmental Biology
- Epigenetics
- Craniofacial Development
Background:
- MLL4 (KMT2D) is an epigenetic regulator vital for organogenesis.
- Mutations in MLL4 cause Kabuki syndrome, characterized by craniofacial defects including palatal anomalies.
Purpose of the Study:
- To investigate the role of MLL4 in palate development and growth.
- To elucidate the molecular mechanisms underlying MLL4's function in the palate.
Main Methods:
- Generated a conditional knockout mouse model with MLL4 deletion in palatal mesenchyme.
- Utilized micro-CT, histology, gene expression profiling, and immunofluorescence.
- Analyzed palate development from perinatal stages to adulthood.
Main Results:
- Mll4-cKO mice exhibited midfacial hypoplasia and palatal midline defects (widened suture, disrupted rugae).
- A transverse growth deficit in palate width was observed.
- Defects included increased apoptosis in the midpalatal suture mesenchyme and impaired chondrogenesis (decreased COL2A1, SOX9).
Conclusions:
- MLL4 is essential for proper midpalatal suture development and overall palate growth.
- MLL4 regulates the expression of key cartilage development genes.
- This study highlights MLL4's critical role in orchestrating cellular and molecular events for normal palate formation.
