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BMP receptor ALK3 controls collecting system development.

Sunny Hartwig1, Darren Bridgewater, Valeria Di Giovanni

  • 1Division of Nephrology, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada.

Journal of the American Society of Nephrology : JASN
|January 8, 2008
PubMed
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Bone morphogenetic protein (BMP) signaling via ALK3 is crucial for normal kidney development. Its deficiency in ureteric buds disrupts branching morphogenesis, leading to kidney dysplasia.

Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Genetics

Background:

  • The molecular mechanisms governing ureteric bud growth and branching during kidney formation are not fully understood.
  • Bone morphogenetic protein (BMP) signaling, particularly through the type I BMP receptor ALK3, has been shown to inhibit ureteric bud and collecting duct cell morphogenesis in vitro.

Purpose of the Study:

  • To investigate the in vivo function of the BMP signaling pathway in regulating ureteric bud development.
  • To determine the role of ALK3 in the ureteric bud lineage during kidney formation.

Main Methods:

  • Generation of a murine model with ALK3 deficiency specifically in the ureteric bud lineage (Alk3(UB-/-) mice).
  • Analysis of kidney development and branching morphogenesis in Alk3(UB-/-) mice compared to wild-type controls.

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Main Results:

  • Alk3(UB-/-) kidneys showed abnormal primary ureteric bud branching and an increased number of branches initially.
  • Later stages of development revealed fewer ureteric bud branches and collecting ducts in Alk3(UB-/-) kidneys.
  • Postnatal mice exhibited renal dysplasia, including medullary hypoplasia, reduced medullary collecting ducts, and altered beta-catenin and c-MYC expression.

Conclusions:

  • Normal kidney development necessitates ALK3-dependent BMP signaling.
  • ALK3 signaling plays a critical role in controlling ureteric bud branching during renal organogenesis.