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Bead Aggregation Assays for the Characterization of Putative Cell Adhesion Molecules
Published on: October 17, 2014
Desmosomal cell adhesion in mammalian development
Xing Cheng1, Zhining Den, Peter J Koch
1Department of Dermatology, Baylor College of Medicine, Houston, TX 77030, USA.
Abstract:
Defects in desmosome-mediated cell-cell adhesion can lead to tissue fragility syndromes. Both inherited and acquired diseases caused by desmosomal defects have been described. The two organs that appear most vulnerable to these defects are the skin with its appendages, and the heart. Furthermore, the analysis of genetically engineered mice has led to the discovery that desmosomal proteins are also required for normal embryonic development. Knockout mice for several desmosomal proteins die in utero. Depending on the protein studied, death occurs either around the time of implantation, at mid-gestation or shortly before birth. So far, it appears that structural defects leading to abnormal histo-architecture and tissue fragility are the main cause of death, i.e. there is no evidence that loss of a desmosomal protein would abort specific cell lineages or differentiation programs. Nevertheless, we are only beginning to understand the functions of individual desmosomal proteins during development. This review focuses on the role of desmosomes during mouse embryonic development.
Insights
Desmosome defects cause tissue fragility and embryonic lethality in mice. These cell adhesion proteins are crucial for development, with mutations leading to structural abnormalities and death during gestation.
Area of Science:
- Cell Biology
- Developmental Biology
- Genetics
Background:
- Desmosomes are critical for cell-cell adhesion and tissue integrity.
- Defects in desmosomes cause inherited and acquired tissue fragility syndromes, primarily affecting skin and heart.
- Desmosomal proteins are essential for embryonic development, as evidenced by embryonic lethality in knockout mouse models.
Purpose of the Study:
- To review the essential roles of desmosomes during mouse embryonic development.
- To highlight the consequences of desmosomal protein loss on embryonic viability and tissue architecture.
Main Methods:
- Analysis of genetically engineered mouse models with targeted desmosomal protein knockouts.
- Examination of embryonic lethality timing and developmental defects in mutant mice.
Main Results:
- Loss of various desmosomal proteins results in embryonic lethality at different developmental stages (implantation, mid-gestation, late gestation).
- Primary cause of death appears to be structural defects leading to abnormal histo-architecture and tissue fragility.
- No evidence suggests that desmosomal protein loss aborts specific cell lineages or differentiation programs.
Conclusions:
- Desmosomes play a vital, non-redundant role in mouse embryonic development.
- Understanding desmosome function is crucial for comprehending developmental processes and associated pathologies.
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