Conditional and inducible transgene expression in mice through the combinatorial use of Cre-mediated recombination and tetracycline induction

Belteki, Gusztav; Haigh, Jody J.; Kabacs, Nikolett; Haigh, Katharina; Sison, Karen; Costantini, Frank; Whitsett, J. A.; Quaggin, Susan E.; Nagy, András

doi:10.1093/nar/gki559

Cited by 100 publications

(128 citation statements)

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“…All mice used in these studies were housed at the University of Michigan mouse facility and were maintained according to the University of Michigan's Committee on Use and Care of Animals (UCUCA)'s protocols. ShhCre, Sox9CreER, Sox9 Flox , β-Catenin Flox , Rosa-rtTa, SftpC-rtTa, Lrp5/6 Flox , and Sox9-eGFP mice have all been previously described (35,36,45,(80)(81)(82). Description of the Rosa26-tetO-Sox9 mice is currently under review elsewhere (Philip A. Seymour, Hung Ping Shih, Richard Behringer, Mark Magnuson, and Maike Sander).…”

Section: Methodsmentioning

confidence: 99%

Sox9 plays multiple roles in the lung epithelium during branching morphogenesis

Rockich¹,

Hrycaj

Shih

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

248

261

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Lung branching morphogenesis is a highly orchestrated process that gives rise to the complex network of gas-exchanging units in the adult lung. Intricate regulation of signaling pathways, transcription factors, and epithelial-mesenchymal cross-talk are critical to ensuring branching morphogenesis occurs properly. Here, we describe a role for the transcription factor Sox9 during lung branching morphogenesis. Sox9 is expressed at the distal tips of the branching epithelium in a highly dynamic manner as branching occurs and is down-regulated starting at embryonic day 16.5, concurrent with the onset of terminal differentiation of type 1 and type 2 alveolar cells. Using epithelial-specific genetic loss-and gain-of-function approaches, our results demonstrate that Sox9 controls multiple aspects of lung branching. Fine regulation of Sox9 levels is required to balance proliferation and differentiation of epithelial tip progenitor cells, and loss of Sox9 leads to direct and indirect cellular defects including extracellular matrix defects, cytoskeletal disorganization, and aberrant epithelial movement. Our evidence shows that unlike other endoderm-derived epithelial tissues, such as the intestine, Wnt/β-catenin signaling does not regulate Sox9 expression in the lung. We conclude that Sox9 collectively promotes proper branching morphogenesis by controlling the balance between proliferation and differentiation and regulating the extracellular matrix.organogenesis | campomelic dysplasia

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Section: Methodsmentioning

confidence: 99%

Sox9 plays multiple roles in the lung epithelium during branching morphogenesis

Rockich¹,

Hrycaj

Shih

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

248

261

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“…For these alleles, it will be necessary to express the blockers in an inducible manner from the population of cells marked with GIFM. One approach that has been developed is activation of tTA or rtTA from a loxP-STOP allele (Park et al, 2004;Belteki et al, 2005;Yu et al, 2005). The neural activity blocker would then be expressed from a tetO phenotyping responder allele.…”

Section: Future Prospects For Using Gifm To Analyze Cell Morphology mentioning

confidence: 99%

Genetic inducible fate mapping in mouse: Establishing genetic lineages and defining genetic neuroanatomy in the nervous system

Joyner

Zervas

2006

Developmental Dynamics

172

167

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A fascinating aspect of developmental biology is how organs are assembled in three dimensions over time. Fundamental to understanding organogenesis is the ability to determine when and where specific cell types are generated, the lineage of each cell, and how cells move to reside in their final position. Numerous methods have been developed to mark and follow the fate of cells in various model organisms used by developmental biologists, but most are not readily applicable to mouse embryos in utero because they involve physical marking of cells through injection of tracers. The advent of sophisticated transgenic and gene targeting techniques, combined with the use of site-specific recombinases, has revolutionized fate mapping studies in mouse. Furthermore, using genetic fate mapping to mark cells has opened up the possibility of addressing fundamental questions that cannot be studied with traditional methods of fate mapping in other organisms. Specifically, genetic fate mapping allows both the relationship between embryonic gene expression and cell fate (genetic lineage) to be determined, as well as the link between gene expression domains and anatomy (genetic anatomy) to be established. In this review, we present the ever-evolving development of genetic fate mapping techniques in mouse, especially the recent advance of Genetic Inducible Fate Mapping. We then review recent studies in the nervous system (focusing on the anterior hindbrain) as well as in the limb and with adult stem cells to highlight fundamental developmental processes that can be discovered using genetic fate mapping approaches. We end with a look toward the future at a powerful new approach that combines genetic fate mapping with cellular phenotyping alleles to study cell morphology, physiology, and function using examples from the nervous system. Developmental Dynamics 235:2376 -2385, 2006.

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“…In mice, this system is able to tightly control gene expression by Dox in a spatiotemporal and quantitative manner (Kistner et al, 1996;Hasan et al, 2004). Moreover, this system has been utilized together with the CreLoxP elements in mice to achieve cell type-, tissue-, or lineage-specific expression of rtTA (Belteki et al, 2005;Yu et al, 2005). The Tet-on system was first used in zebrafish for improving GFP expression in a gene-trap vector.…”

Section: Introductionmentioning

confidence: 99%