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Branching morphogenesis and renal dysplasia

The mammalian kidney develops by a process called branching morphogenesis, which is driven by reciprocal inductive interactions between the metanephric blastema and ureteric bud (UB) embryonic tissue. To further investigate the inhibitory role of the BMP2 receptor ALK3 in kidney branching morphogenesis, Hu et al. generated mice expressing a constitutively active form of ALK3 in the UB (see p. 2753). As expected, mutant kidneys undergo less branching, but this surprisingly leads to medullary cystic dysplasia rather than to kidney hypoplasia. The transition from decreased branching to cystic dysplasia is accompanied by the increased expression of ß-catenin and TCF, and by the formation of ß-catenin/SMAD1 (an ALK3 effector) complexes. As such, ALK3 signalling appears to upregulate ß-catenin expression via an unknown mechanism during this pathogenic event, providing new directions for studies of human renal dysplasia.

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Elevated SMAD1/ß-catenin molecular complexes and renal medullary cystic dysplasia in ALK3 transgenic mice

Ming Chang Hu, Tino D. Piscione, and Norman D. Rosenblum
Development 2003 130: 2753-2766. [Abstract] [Full Text]  

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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Search for Related Content