Unifying the p73 knockout phenotypes: TAp73 orchestrates multiciliogenesis
- Marco Napoli1,2 and
- Elsa R. Flores1,2,3
- 1Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA
- 2Department of Translational Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA
- 3Graduate School of Biomedical Sciences, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA
- Corresponding author: elsaflores{at}mdanderson.org
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.
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Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.283663.116.
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