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Conditional Reprogramming of Pediatric Human Esophageal Epithelial Cells for Use in Tissue Engineering and Disease Investigation
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p73 and FoxJ1: Programming Multiciliated Epithelia.

Peter K Jackson1, Laura D Attardi2

  • 1Stanford University School of Medicine, Baxter Laboratory, Departments of Microbiology and Immunology and Pathology, Stanford, CA 94305, USA.

Trends in Cell Biology
|March 19, 2016
PubMed
Summary
This summary is machine-generated.

The tumor suppressor p73 (p53 homolog) is essential for developing multiciliated epithelia. New analysis reveals p73 directly activates FoxJ1, a key gene for ciliogenesis, unifying diverse p73-deficient mouse phenotypes.

Keywords:
Primary ciliadifferentiationmulticiliated epitheliap53p63p73

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • The p53 homolog p73 plays a role in diverse cellular processes.
  • Mice lacking p73 exhibit varied developmental abnormalities, the underlying cause of which was previously unclear.

Purpose of the Study:

  • To elucidate the unifying mechanism behind the diverse phenotypes observed in p73-deficient mice.
  • To investigate the role of p73 in the development of multiciliated epithelia.

Main Methods:

  • Analysis of gene expression patterns in p73-deficient mice.
  • Investigating the regulatory relationship between p73 and the FoxJ1 gene.

Main Results:

  • p73 is demonstrated to be indispensable for the formation of multiciliated epithelia.
  • p73 directly activates the transcription factor FoxJ1, a critical regulator of multiciliation.
  • p73 induces numerous genes essential for the process of ciliogenesis.

Conclusions:

  • The requirement of p73 for multiciliated epithelial development unifies previously disparate observations in p73 knockout models.
  • p73 acts as a crucial upstream regulator of the FoxJ1-mediated transcriptional network governing ciliogenesis.