Abstract
Branching morphogenesis, defined as growth and branching of epithelial tubules during embryogenesis, is a fundamental feature of renal, lung, mammary gland, submandibular gland, and pancreatic morphogenesis in mammals. Disruption of branching morphogenesis has been demonstrated to result in maldevelopment of some of these organs. Genetic studies performed in affected humans and mutant mice have implicated transcription factors, secreted growth factors, and cell surface signaling molecules as critical regulators of branching morphogenesis. These factors function within networks that appear to exert tight control over the number and location of branches. This review summarizes current knowledge regarding the molecular control of branching morphogenesis in vivo with particular emphasis on the genetic contribution to perturbed branching morphogenesis in mice and humans.
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Abbreviations
- FGF:
-
fibroblast growth factor
- BMP:
-
bone morphogenetic protein
- ALK:
-
activin-like kinase
- SHH:
-
sonic hedgehog
- EGF:
-
epidermal growth factor
- FGFR:
-
fibroblast growth factor receptor
- EGFR:
-
epidermal growth factor receptor
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This review is the eighth in this series. Drs. Hu and Rosenblum describe the genetic control of branching morphogenesis and the central role of epithelial-mesenchyme interaction. The review contains descriptions of animal models and human disorders resulting from specific genetic defects. Branching morphogenesis is a fundamental process in human developmental biology and this review describes the process and its control in many organs of the body, including kidney, pancreas, lung, breast and salivary glands.
Alvin Zipursky
Editor-in-Chief
Supported by operating funds awarded to N.D.R. by the Canadian Institutes of Health Research and the Kidney Foundation of Canada.
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Hu, M., Rosenblum, N. Genetic Regulation of Branching Morphogenesis: Lessons Learned from Loss-of-Function Phenotypes. Pediatr Res 54, 433–438 (2003). https://doi.org/10.1203/01.PDR.0000085170.44226.DB
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DOI: https://doi.org/10.1203/01.PDR.0000085170.44226.DB
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