Activin disrupts epithelial branching morphogenesis in developing glandular organs of the mouse

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 caus...

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Bibliographic Details
Published in:Mechanisms of development 1995-04, Vol.50 (2), p.229-245
Main Authors: Ritvos, Olli, Tuuri, Timo, Erämaa, Marja, Sainio, Kirsi, Hildén, Kristiina, Saxén, Lauri, Gilbert, Scott F.
Format: Article
Language:English
Subjects:
Activin
Activin Receptors
Activins
Amino Acid Sequence
Animals
Base Sequence
Embryonic and Fetal Development - drug effects
Epithelial branching morphogenesis
Follistatin
Glycoproteins - genetics
Growth Substances - toxicity
Humans
Inhibins - genetics
Inhibins - toxicity
Kidney - drug effects
Kidney - embryology
Mice
Mice, Inbred CBA
Molecular Sequence Data
Morphogenesis - drug effects
Mouse embryogenesis
Organ Culture Techniques
Pancreas - drug effects
Pancreas - embryology
Receptors, Growth Factor - genetics
RNA, Messenger - biosynthesis
Salivary Glands - drug effects
Salivary Glands - embryology
TGF-β
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Summary: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-β 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.
ISSN:0925-4773
1872-6356
DOI:10.1016/0925-4773(94)00342-K