| Temporal control of gene recombination in astrocytes by transgenic expression of the tamoxifen-inducible DNA recombinase variant CreERT2. | |
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MedLine Citation:
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PMID: 16575885 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Inducible gene modification using the Cre/loxP system provides a valuable tool for the analysis of gene function in the active animal. GFAP-Cre transgenic mice have been developed to achieve gene recombination in astrocytes, the most abundant cells of the central nervous system, with pivotal roles during brain function and pathology. Unfortunately, these mice displayed neuronal recombination as well, since the GFAP promoter is also active in embryonic radial glia, which possess a substantial neurogenic potential. To enable the temporal control of gene deletions in astrocytes only, we generated a transgenic mouse with expression of CreERT2, a fusion protein of the DNA recombinase Cre and a mutated ligand-binding domain of the estrogen receptor, under the control of the human GFAP promoter. In offspring originating from crossbreedings of GFAP-CreERT2-transgenic mice with various Cre-sensitive reporter mice, consecutive intraperitoneal injections of tamoxifen induced genomic recombination selectively in astrocytes of almost all brain regions. In Bergmann glia, which represent the main astroglial cell population of the cerebellum, virtually all cells showed successful gene recombination. When adult mice received cortical stab wound lesions, simultaneously given tamoxifen induced substantial recombination in reactive glia adjacent to the site of injury. These transgenic GFAP-CreERT2 mice will allow the functional analysis of loxP-modified genes in astroglia of the postnatal and adult brain. |
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Authors:
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Petra G Hirrlinger; Anja Scheller; Christian Braun; Johannes Hirrlinger; Frank Kirchhoff |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Glia Volume: 54 ISSN: 0894-1491 ISO Abbreviation: Glia Publication Date: 2006 Jul |
Date Detail:
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Created Date: 2006-05-25 Completed Date: 2006-07-27 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 8806785 Medline TA: Glia Country: United States |
Other Details:
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Languages: eng Pagination: 11-20 Citation Subset: IM |
Copyright Information:
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Copyright 2005 Wiley-Liss, Inc. |
Affiliation:
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Department of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antineoplastic Agents, Hormonal / pharmacology Astrocytes / cytology, metabolism* Brain / cytology, growth & development, metabolism Brain Injuries / genetics, metabolism, physiopathology Cells, Cultured Disease Models, Animal Female Gene Deletion Gene Expression Regulation, Developmental / genetics* Glial Fibrillary Acidic Protein / genetics Gliosis / genetics, metabolism, physiopathology Humans Integrases / genetics* Male Mice Mice, Inbred C57BL Mice, Transgenic Promoter Regions, Genetic / genetics Receptors, Estrogen / genetics* Recombinant Fusion Proteins / biosynthesis, genetics* Recombination, Genetic / genetics* Tamoxifen / pharmacology Time Factors Transgenes / genetics Viral Proteins / genetics* |
| Chemical | |
Reg. No./Substance:
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0/Antineoplastic Agents, Hormonal; 0/Glial Fibrillary Acidic Protein; 0/Receptors, Estrogen; 0/Recombinant Fusion Proteins; 0/Viral Proteins; 10540-29-1/Tamoxifen; EC 2.7.7.-/Cre recombinase; EC 2.7.7.-/Integrases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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