Embryonic defects and growth alteration in mice with homozygous disruption of the Patz1 gene1. Issue 3 (23rd November 2012)

• Record Type: Journal Article
• Authors: Valentino, Teresa; Palmieri, Dario; Vitiello, Michela; Simeone, Antonio; Palma, Giuseppe; Arra, Claudio; Chieffi, Paolo; Chiariotti, Lorenzo; Fusco, Alfredo; Fedele, Monica
• Is Part Of: Journal of cellular physiology. Volume 228:Issue 3(2013:Mar.)
• Page Start: 646
• Page End: 653
• Publication Date: 2012-11-23
• Subjects: Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.24174
• Languages: English
• ISSNs: 0021-9541

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <p> <italic>PATZ1</italic> 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 <italic>Patz1</italic> 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 <italic>Patz1</italic> 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. J. Cell. Physiol. 228: 646–653, 2013. © 2012 Wiley Periodicals, Inc.</p> </abstract>