Rescue of key features of the p63-null epithelial phenotype by inactivation of Ink4a and Arf
Mice lacking p63 cannot form skin, exhibit craniofacial and skeletal defects, and die soon after birth. The p63 gene regulates a complex network of target genes, and disruption of p63 has been shown to affect the maintenance of epithelial stem cells, the differentiation of keratinocytes, and the pre...
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| Published in | The EMBO journal Vol. 28; no. 13; pp. 1904 - 1915 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Chichester, UK
John Wiley & Sons, Ltd
08.07.2009
Blackwell Publishing Ltd Nature Publishing Group |
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| Online Access | Get full text |
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| Abstract | Mice lacking p63 cannot form skin, exhibit craniofacial and skeletal defects, and die soon after birth. The p63 gene regulates a complex network of target genes, and disruption of p63 has been shown to affect the maintenance of epithelial stem cells, the differentiation of keratinocytes, and the preservation of the adhesive properties of stratified epithelium. Here, we show that inactivation of p63 in mice is accompanied by aberrantly increased expression of the Ink4a and Arf tumour suppressor genes. In turn, anomalies of the p63‐null mouse affecting the skin and skeleton are partially ameliorated in mice lacking either Ink4a or Arf. Rescue of epithelialization is accompanied by restoration of keratinocyte proliferative capacity both in vivo and in vitro and by expression of markers of squamous differentiation. Thus, in the absence of p63, abnormal upregulation of Ink4a and Arf is incompatible with skin development. |
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| AbstractList | Mice lacking p63 cannot form skin, exhibit craniofacial and skeletal defects, and die soon after birth. The p63 gene regulates a complex network of target genes, and disruption of p63 has been shown to affect the maintenance of epithelial stem cells, the differentiation of keratinocytes, and the preservation of the adhesive properties of stratified epithelium. Here, we show that inactivation of p63 in mice is accompanied by aberrantly increased expression of the Ink4a and Arf tumour suppressor genes. In turn, anomalies of the p63-null mouse affecting the skin and skeleton are partially ameliorated in mice lacking either Ink4a or Arf. Rescue of epithelialization is accompanied by restoration of keratinocyte proliferative capacity both in vivo and in vitro and by expression of markers of squamous differentiation. Thus, in the absence of p63, abnormal upregulation of Ink4a and Arf is incompatible with skin development. Mice lacking p63 cannot form skin, exhibit craniofacial and skeletal defects, and die soon after birth. The p63 gene regulates a complex network of target genes, and disruption of p63 has been shown to affect the maintenance of epithelial stem cells, the differentiation of keratinocytes, and the preservation of the adhesive properties of stratified epithelium. Here, we show that inactivation of p63 in mice is accompanied by aberrantly increased expression of the Ink4a and Arf tumour suppressor genes. In turn, anomalies of the p63-null mouse affecting the skin and skeleton are partially ameliorated in mice lacking either Ink4a or Arf. Rescue of epithelialization is accompanied by restoration of keratinocyte proliferative capacity both in vivo and in vitro and by expression of markers of squamous differentiation. Thus, in the absence of p63, abnormal upregulation of Ink4a and Arf is incompatible with skin development. [PUBLICATION ABSTRACT] Mice lacking p63 cannot form skin, exhibit craniofacial and skeletal defects, and die soon after birth. The p63 gene regulates a complex network of target genes, and disruption of p63 has been shown to affect the maintenance of epithelial stem cells, the differentiation of keratinocytes, and the preservation of the adhesive properties of stratified epithelium. Here, we show that inactivation of p63 in mice is accompanied by aberrantly increased expression of the Ink4a and Arf tumour suppressor genes. In turn, anomalies of the p63 -null mouse affecting the skin and skeleton are partially ameliorated in mice lacking either Ink4a or Arf . Rescue of epithelialization is accompanied by restoration of keratinocyte proliferative capacity both in vivo and in vitro and by expression of markers of squamous differentiation. Thus, in the absence of p63 , abnormal upregulation of Ink4a and Arf is incompatible with skin development. |
| Author | Flores, Elsa R Gi, Young-Jin Ayanga, Bernard A Cho, Min Soon Sherr, Charles J Su, Xiaohua |
| Author_xml | – sequence: 1 givenname: Xiaohua surname: Su fullname: Su, Xiaohua organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, TX, Houston, USA – sequence: 2 givenname: Min Soon surname: Cho fullname: Cho, Min Soon organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA – sequence: 3 givenname: Young-Jin surname: Gi fullname: Gi, Young-Jin organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, TX, Houston, USA – sequence: 4 givenname: Bernard A surname: Ayanga fullname: Ayanga, Bernard A organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, TX, Houston, USA – sequence: 5 givenname: Charles J surname: Sherr fullname: Sherr, Charles J organization: Howard Hughes Medical Institute, Genetics and Tumor Cell Biology, St Jude Children's Research Hospital, Memphis, TN, USA – sequence: 6 givenname: Elsa R surname: Flores fullname: Flores, Elsa R email: elsaflores@mdanderson.org organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA |
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| Copyright | Copyright © 2009 European Molecular Biology Organization Copyright Nature Publishing Group Jul 8, 2009 Copyright © 2009, European Molecular Biology Organization 2009 |
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| Snippet | Mice lacking p63 cannot form skin, exhibit craniofacial and skeletal defects, and die soon after birth. The p63 gene regulates a complex network of target... Mice lacking p63 cannot form skin, exhibit craniofacial and skeletal defects, and die soon after birth. The p63 gene regulates a complex network of target... |
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| SubjectTerms | adhesion ADP-Ribosylation Factors - genetics ADP-Ribosylation Factors - metabolism Animals Cell Differentiation Cell Proliferation Cells, Cultured Cyclin-Dependent Kinase Inhibitor p16 - genetics Cyclin-Dependent Kinase Inhibitor p16 - metabolism differentiation epidermal stem cells Female Gene expression Gene Expression Regulation, Developmental Genotype & phenotype Inactivation Ink4a-Arf Keratinocytes - cytology Mice Mice, Inbred C57BL Mice, Knockout Molecular biology p63-isoforms Phenotype Phosphoproteins - genetics Phosphoproteins - metabolism Pregnancy Rodents Skin Skin - cytology Skin - embryology Skin - metabolism Stem cells Trans-Activators - genetics Trans-Activators - metabolism |
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| Title | Rescue of key features of the p63-null epithelial phenotype by inactivation of Ink4a and Arf |
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