Related Experiment Video
Updated: Jul 4, 2025
07:45
An Explant Assay for Assessing Cellular Behavior of the Cranial Mesenchyme
Published on: January 20, 2013
9.8K
Grainyhead-like 2 interacts with noggin to regulate tissue fusion in mouse
Michael E de Vries1,2, Marina R Carpinelli1, Jarrad N Fuller2
1Department of Medicine, Monash University Central Clinical School, Prahran, Victoria 3004, Australia.
Development (Cambridge, England)
|February 1, 2024
Summary
Defective tissue fusion in mammalian development, linked to grainyhead-like 2 (Grhl2) deficiency, involves the bone morphogenetic protein (BMP) inhibitor noggin (NOG). Reducing NOG partially rescues fusion defects, suggesting NOG
Area of Science:
- Developmental biology
- Molecular genetics
- Congenital anomalies
Background:
- Defective tissue fusion during mammalian embryogenesis leads to congenital anomalies like cleft lip/palate.
- Grainyhead-like 2 (Grhl2) is a key transcription factor regulating tissue fusion.
- Grhl2-deficient mice exhibit severe developmental defects, including neural tube and facial clefting.
Purpose of the Study:
- To investigate the interaction between Grhl2 and noggin (NOG) in mammalian tissue fusion.
- To elucidate the role of BMP signaling in Grhl2-mediated craniofacial development.
- To determine if modulating NOG levels can rescue Grhl2-deficiency-related defects.
Main Methods:
- Analysis of Grhl2-deficient mouse embryos (Grhl2-/-).
- Assessment of NOG expression and BMP signaling pathway activation (pSMAD5).
- Generation and analysis of compound mutant embryos (Grhl2-/-;Nog+/-).
Main Results:
- Grhl2 deficiency causes maxillary prominence epithelial abnormalities and NOG upregulation.
- BMP signaling is disrupted in Grhl2-deficient craniofacial tissues.
- Reducing NOG levels in Grhl2-/- embryos partially rescues tissue fusion and craniofacial morphology.
Conclusions:
- Grhl2 regulates tissue fusion, partly through the modulation of NOG expression.
- Aberrant epithelial maintenance, influenced by NOG-mediated BMP-SMAD pathway regulation, contributes to fusion defects in Grhl2-/- mice.
- Targeting NOG may offer therapeutic potential for congenital fusion anomalies.
Related Concept Videos
01:56Gastrulation
57.4K
Gastrulation establishes the three primary tissues of an embryo: the ectoderm, mesoderm, and endoderm. This developmental process relies on a series of intricate cellular movements, which in humans transforms a flat, “bilaminar disc” composed of two cell sheets into a three-tiered structure. In the resulting embryo, the endoderm serves as the bottom layer, and stacked directly above it is the intermediate mesoderm, and then the uppermost ectoderm. Respectively, these tissue strata...
57.4K
03:14Notch Signaling Pathway
4.3K
The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
4.3K
01:30Neurulation
41.9K
Neurulation is the embryological process which forms the precursors of the central nervous system and occurs after gastrulation has established the three primary cell layers of the embryo: ectoderm, mesoderm, and endoderm. In humans, the majority of this system is formed via primary neurulation, in which the central portion of the ectoderm—originally appearing as a flat sheet of cells—folds upwards and inwards, sealing off to form a hollow neural tube. As development proceeds, the...
41.9K