Unifying the p73 knockout phenotypes: TAp73 orchestrates multiciliogenesis

Genes Dev. 2016 Jun 1;30(11):1253-4. doi: 10.1101/gad.283663.116.

Abstract

Multiciliogenesis is essential for the function of different epithelia, and its failure results in brain defects, respiratory diseases, and infertility. In this issue of Genes & Development, Nemajerova and colleagues (pp. 1300-1312) reveal the p53 family member and p73 isoform TAp73 as a transcription factor dictating the differentiation of multiciliated cells. Their findings provide the long-awaited unifying explanation for the diverse phenotypes of the p73 knockout mice.

Keywords: TAp73; TP73; airways; central transcriptional regulator; motile multiciliogenesis; p73.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Cell Differentiation
  • DNA-Binding Proteins / genetics
  • Nuclear Proteins / genetics*
  • Phenotype
  • Transcription Factors / genetics
  • Tumor Protein p73*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Proteins / genetics

Substances

  • DNA-Binding Proteins
  • Nuclear Proteins
  • Transcription Factors
  • Tumor Protein p73
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins