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Related Experiment Videos

Stromal cells mediate retinoid-dependent functions essential for renal development.

C Mendelsohn1, E Batourina, S Fung

  • 1Columbia University, Department of Urology, New York, NY 10032, USA. clm20@columbia.edu

Development (Cambridge, England)
|February 18, 1999
PubMed
Summary

Retinoic acid receptors alpha and beta2 are crucial for embryonic kidney development. Their combined absence impairs ureteric bud branching by downregulating c-ret signaling in stromal cells, leading to renal malformations.

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Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Genetics

Background:

  • Vitamin A metabolites, retinoids, are essential for kidney development.
  • Retinoids signal through retinoic acid receptors (RARs) and retinoid X receptors (RXRs).
  • Previous studies indicated RARalpha and RARbeta2 receptors are vital for renal morphogenesis.

Purpose of the Study:

  • To investigate the specific roles of RARalpha and RARbeta2 in embryonic kidney development.
  • To elucidate the cellular localization and functional interactions of RARalpha and RARbeta2 in the developing kidney.

Main Methods:

  • Gene targeting to create RARalpha beta2 double knockout mice.
  • Histological analysis of embryonic kidneys.
  • Immunohistochemistry to determine receptor localization.

Related Experiment Videos

  • Gene expression analysis of key developmental markers.

    • Main Results:

    • RARalpha and RARbeta2 are co-localized in embryonic kidney stromal cells.
    • RARalpha beta2 mutant kidneys exhibit impaired ureteric bud branching and collecting duct development.
    • Nephron formation is unaffected, but ureteric bud tips are abnormally positioned.
    • Downregulation of the proto-oncogene c-ret was observed in mutant kidneys.

    Conclusions:

    • RARalpha and RARbeta2 in stromal cells are essential for maintaining c-ret expression.
    • This stromal cell-mediated c-ret signaling is critical for proper ureteric bud morphogenesis.
    • Disruption of this pathway leads to renal malformations due to impaired branching.