Embryonic defects and growth alteration in mice with homozygous disruption of the Patz1 gene

Teresa Valentino, Dario Palmieri, Michela Vitiello, Antonio Simeone, Giuseppe Palma, Claudio Arra, Paolo Chieffi, Lorenzo Chiariotti, Alfredo Fusco, Monica Fedele

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PATZ1 is an emerging cancer-related gene coding for a POZ/AT-hook/kruppel Zinc finger transcription factor, which is lost or misexpressed in human neoplasias. Here, we investigated its role in development exploring wild-type and Patz1-knockout mice during embryogenesis. We report that the Patz1 gene is ubiquitously expressed at early stages of development and becomes more restricted at later stages, with high levels of expression in actively proliferating neuroblasts belonging to the ventricular zones of the central nervous system (CNS). The analysis of embryos in which Patz1 was disrupted revealed the presence of severe defects in the CNS and in the cardiac outflow tract, which eventually lead to a pre-mature in utero death during late gestation or soon after birth. Moreover, the Patz1-null mice showed a general growth retardation, which was consistent with the slower growth rate and the increased susceptibility to senescence of Patz1-/- mouse embryonic fibroblasts (MEFs) compared to wild-type controls. Therefore, these results indicate a critical role of PATZ1 in the control of cell growth and embryonic development.

Original languageEnglish
Pages (from-to)646-653
Number of pages8
JournalJournal of Cellular Physiology
Issue number3
Publication statusPublished - Mar 2013

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology


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