Mice with the Enhanced Green Fluorescent Protein Gene Knocked in to Chromosome 11 Exhibit Normal Transmission Ratios

Kłysik, Jan; Singer, Jeffrey D.

doi:10.1007/s10528-005-5223-6

Cited by 5 publications

(3 citation statements)

References 32 publications

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“…200 G418-resistant clones were selected for further analysis. Correctly targeted ES cell clones (Figure 1B and 1C) were identified as described (Klysik and Singer 2005; Ramirez-Solis et al 1995). …”

Section: Methodsmentioning

confidence: 90%

Disruption of Supv3L1 damages the skin and causes sarcopenia, loss of fat, and death

et al. 2009

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Supv3L1 is a conserved and ubiquitously expressed helicase found in numerous tissues and cell types of many species. In human cells, SUPV3L1 was shown to suppress apoptotic death, sister chromatid exchange, and impair mitochondrial RNA metabolism and protein synthesis. In vitro experiments revealed binding of SUPV3L1 to BLM and WRN proteins suggesting a role in genome maintenance processes. Disruption of the Supv3L1 gene in the mouse has been reported to be embryonic lethal at early developmental stages. We generated a conditional mouse in which the phenotypes associated with the removal of exon 14 can be tested in a variety of tissues. Disruption mediated by a Mx1 promoter-driven Cre displayed a postnatal growth delay, reduced life span, loss of adipose tissue, muscle mass, and severe skin abnormalities manifesting as ichthyosis, thickening of the epidermis, and atrophy of the dermis and subcutaneous tissue. Using a tamoxifen-activatable Esr1/Cre driver, Supv3L1 disruption resulted in growth retardation and aging phenotypes including loss of adipose tissue, muscle mass, kyphosis, cachexia and premature death. Many of the abnormalities seen in the Mx1-Cre mice, such as hyperkeratosis characterized by profound scaling of feet and tail, could also be detected in tamoxifen-inducible Cre mice. Conditional ablation of Supv3L1 in keratinocytes confirmed atrophic changes in the skin and ichthyosis-like changes. Together, these data indicate that Supv3L1 is important for the maintenance of the skin barrier. Additionally, loss of Supv3L1 function leads to accelerated aging-like phenotypes.

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Section: Methodsmentioning

confidence: 90%

Disruption of Supv3L1 damages the skin and causes sarcopenia, loss of fat, and death

et al. 2009

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“…The exact nature of the genetic lesion can be subtle (such as small deletions or point mutations) and therefore often hard to pinpoint. The use of highly transposable elements and other selective tricks has facilitated forward genetic screening of mice [15][16][17][18]. The development of mouse embryonic stem cells has led to important progress in the generation of gene-targeted genetically engineered mice.…”

Section: Gene Targetingmentioning

confidence: 99%

Controlled and localized genetic manipulation in the brain

Aronoff

Petersen

2006

Journal of Cellular and Molecular Medicine

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Establishing the contributions of inherited genes relative to experience in brain function forms a central theme of neuroscience. There is little doubt that both activity-dependent neuronal plasticity and genetically determined programs generate important influences on the developing and the adult nervous system. The ability to change behaviour in response to new environmental hazards and AbstractBrain structure and function are determined in part through experience and in part through our inherited genes. A powerful approach for unravelling the balance between activity-dependent neuronal plasticity and genetic programs is to directly manipulate the genome. Such molecular genetic studies have been greatly aided by the remarkable progress of large-scale genome sequencing efforts. Sophisticated mouse genetic manipulations allow targeted point-mutations, deletions and additions to the mouse genome. These can be regulated through inducible promoters expressing in genetically specified neuronal cell types. However, despite significant progress it remains difficult to target specific brain regions through transgenesis alone. Recent work suggests that transduction vectors, like lentiviruses and adeno-associated viruses, may provide suitable additional tools for localized and controlled genetic manipulation. Furthermore, studies with such vectors may aid the development of human genetic therapies for brain diseases.

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“…Correctly targeted ES cell clones (Fig. 1B and C) were identified as described (Ramirez-Solis et al 1995; Klysik and Singer 2005). …”

Section: Methodsmentioning

confidence: 99%

Widespread expression of the Supv3L1 mitochondrial RNA helicase in the mouse

et al. 2009

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Supv3L1 is an evolutionarily conserved helicase that plays a critical role in the mitochondrial RNA surveillance and degradation machinery. Conditional ablation of Supv3L1 in adult mice leads to premature aging phenotypes including loss of muscle mass and adipose tissue and severe skin abnormalities. To get insights into the spatial and temporal expression of Supv3L1 in the mouse, we generated knock-in and transgenic strains in which an EGFP reporter was placed under control of the Supv3L1 native promoter. During development, expression of Supv3L1 begins at the blastocyst stage, becomes widespread and strong in all fetal tissues and cell types, and continues during postnatal growth. In mature animals reporter expression is only slightly diminished in most tissues and continues to be highly expressed in the brain, peripheral sensory organs, and testis. Together, these data confirm that Supv3L1 is an important developmentally regulated gene, which continues to be expressed in all mature tissues, particularly the rapidly proliferating cells of testes, but also in the brain and sensory organs. The transgenic mice and cell lines derived from them constitute a valuable tool for the examination of the spatial and temporal aspects of Supv3L1 promoter activity, and should facilitate future screens for small molecules that regulate Supv3L1 expression.

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Mice with the Enhanced Green Fluorescent Protein Gene Knocked in to Chromosome 11 Exhibit Normal Transmission Ratios

Cited by 5 publications

References 32 publications

Disruption of Supv3L1 damages the skin and causes sarcopenia, loss of fat, and death

Disruption of Supv3L1 damages the skin and causes sarcopenia, loss of fat, and death

Controlled and localized genetic manipulation in the brain

Widespread expression of the Supv3L1 mitochondrial RNA helicase in the mouse

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