Loss of digestive organ expansion factor (Diexf) reveals an essential role during murine embryonic development that is independent of p53
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Neeraj K. Aryal1,2, Amanda R. Wasylishen1, Vinod Pant1, Maurisa Riley-Croce1 and Guillermina Lozano1
1Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
2Genes and Development Program, The University of Texas MD Anderson Cancer Center, UT Health Graduate School of Biomedical Sciences, Houston, TX 77030, USA
Guillermina Lozano, email: [email protected]
Keywords: CRISPR/Cas9; mouse model; ribosome small subunit processome; Mdm4 co-amplification; Def-Capn3 nucleolar pathway
Received: August 15, 2017 Accepted: October 10, 2017 Published: October 26, 2017
Increased levels of inhibitors of the p53 tumor suppressor such as Mdm2 and Mdm4 drive tumor development and thus serve as targets for therapeutic intervention. Recently, digestive organ expansion factor (Diexf) has been identified as a novel inhibitor of p53 in zebrafish. Here, we address the potential role of Diexf as a regulator of the p53 pathway in mammals by generating Diexf knockout mice. We demonstrate that, similar to Mdm2 and Mdm4, homozygous deletion of Diexf is embryonic lethal. However, unlike in Mdm2 and Mdm4 mice, loss of p53 does not rescue this phenotype. Moreover, Diexf heterozygous animals are not sensitive to sub-lethal ionizing radiation. Thus, we conclude that Diexf is an essential developmental gene in the mouse, but is not a significant regulator of the p53 pathway during development or in response to ionizing radiation.
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