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Functional compensation in Hedgehog signaling during mouse prostate development

Jason Doles1, Crist Cook, Xudong Shi

  • 1Department of Surgery, University of Wisconsin-Madison, Box 3236 Clinical Science Center-G5, 600 Highland Avenue, Madison, WI 53792, USA.

Developmental Biology
|May 19, 2006
PubMed

Insights

Hedgehog signaling is crucial for prostate development, but functional redundancy among Gli transcription factors mitigates defects. This study clarifies the complex roles of hedgehog signaling and Gli factors in prostate morphogenesis.

Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Genetics

Background:

  • Hedgehog (Hh) signaling is vital for embryonic development, including prostate morphogenesis.
  • Previous studies on Hh signaling's role in prostate development yielded conflicting results due to varied methodologies.

Purpose of the Study:

  • To elucidate the precise role of Hh signaling in prostate ductal budding and glandular morphogenesis.
  • To investigate the functional redundancy among Gli transcription factors in prostate development.

Main Methods:

  • Utilized transgenic mouse models, chemical inhibitors (cyclopamine), and renal grafting.
  • Analyzed Gli1, Gli2, and Gli3 knockout mouse models for prostate development phenotypes.
  • Assessed Hh pathway activity and prostatic differentiation in mutant Urogenital Sinus (UGS) explants.

Main Results:

  • Genetic loss of Sonic Hedgehog (Shh) led to Indian Hedgehog (Ihh) upregulation and sustained Hh pathway activity.
  • Gli1 and Gli3 are not essential for prostate ductal budding, but Gli2 deficiency caused aberrant budding.
  • Gli2 knockout UGS showed prostatic differentiation with focal hyperplasia; functional redundancy among Gli factors was evident.

Conclusions:

  • Significant functional redundancy exists at both ligand and transcriptional regulatory levels in Hh signaling during prostate development.
  • This redundancy effectively buffers phenotypes resulting from Hh signaling perturbations, explaining previous conflicting data.

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