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Activin disrupts epithelial branching morphogenesis in developing glandular organs of the mouse
1Department of Bacteriology and Immunology, University of Helsinki, Finland.
Abstract:
We report that activin profoundly alters epithelial branching morphogenesis of embryonic mouse salivary gland, pancreas and kidney rudiments in culture, indicating that it may play a role as a morphogen during mammalian organogenesis. In developing pancreas and salivary gland rudiments, activin causes severe disruption of normal lobulation patterns of the epithelium whereas follistatin, an activin-binding protein, counteracts the effect of activin. In the kidney, activin delays branching of the ureter bud and reduces the number of secondary branches. TGF-beta induces a pattern of aberrant branching in the ureter bud derived epithelium distinct from that seen for activin. Reverse-transcriptase polymerase chain reaction, Northern hybridization and in situ hybridization analyses indicate that these developing tissues express the mRNA transcripts for activin subunits, follistatin or activin receptors. Our results are suggestive of a potential role for the activin-follistatin system as an intrinsic regulator of epithelial branching morphogenesis during mammalian organogenesis.
Insights
Activin significantly impacts epithelial branching morphogenesis in developing mouse organs, including salivary glands, pancreas, and kidneys. The activin-follistatin system may act as an intrinsic regulator during mammalian organogenesis.
Area of Science:
- Developmental Biology
- Molecular Biology
- Cell Biology
Background:
- Epithelial branching morphogenesis is crucial for mammalian organ development.
- The role of specific signaling pathways, like activin, in this process is not fully understood.
Purpose of the Study:
- To investigate the role of activin in epithelial branching morphogenesis of embryonic mouse salivary gland, pancreas, and kidney rudiments.
- To explore the potential involvement of the activin-follistatin system in mammalian organogenesis.
Main Methods:
- Organ culture of embryonic mouse salivary gland, pancreas, and kidney rudiments.
- Treatment with activin and follistatin.
- Analysis of branching patterns and lobulation.
- Gene expression analysis using reverse-transcriptase polymerase chain reaction, Northern hybridization, and in situ hybridization.
Main Results:
- Activin profoundly altered epithelial branching morphogenesis in all studied organs.
- Activin disrupted normal lobulation in pancreas and salivary gland, an effect counteracted by follistatin.
- In kidneys, activin delayed ureter bud branching and reduced secondary branches.
- Developing tissues expressed mRNA for activin subunits, follistatin, and activin receptors.
Conclusions:
- Activin plays a significant role in regulating epithelial branching morphogenesis during mammalian organogenesis.
- The activin-follistatin system appears to function as an intrinsic regulator of this developmental process.