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A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme
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| Zeitschriftentitel: | genesis |
|---|---|
| Personen und Körperschaften: | , , , |
| In: | genesis, 48, 2010, 3, S. 207-212 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Inoue, Shuji Inoue, Miki Fujimura, Sayoko Nishinakamura, Ryuichi Inoue, Shuji Inoue, Miki Fujimura, Sayoko Nishinakamura, Ryuichi |
|---|---|
| author |
Inoue, Shuji Inoue, Miki Fujimura, Sayoko Nishinakamura, Ryuichi |
| spellingShingle |
Inoue, Shuji Inoue, Miki Fujimura, Sayoko Nishinakamura, Ryuichi genesis A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme Cell Biology Endocrinology Genetics |
| author_sort |
inoue, shuji |
| spelling |
Inoue, Shuji Inoue, Miki Fujimura, Sayoko Nishinakamura, Ryuichi 1526-954X 1526-968X Wiley Cell Biology Endocrinology Genetics http://dx.doi.org/10.1002/dvg.20603 <jats:title>Abstract</jats:title><jats:p><jats:italic>Sall1</jats:italic> is expressed in the metanephric mesenchyme in the developing kidney, and mice deficient in <jats:italic>Sall1</jats:italic> show kidney agenesis or dysgenesis. <jats:italic>Sall1</jats:italic> is also expressed elsewhere, including in the limb buds, anus, heart, and central nervous system. Dominant‐negative mutations of <jats:italic>Sall1</jats:italic> in mice and humans lead to developmental defects in these organs. Here, we generated a mouse line expressing tamoxifen‐inducible Cre recombinase (<jats:italic>CreER<jats:sup>T2</jats:sup></jats:italic>) under the control of the endogenous Sall1 promoter. Upon tamoxifen treatment, these mice showed genomic recombination in the tissues where endogenous <jats:italic>Sall1</jats:italic> is expressed. When <jats:italic>CreER<jats:sup>T2</jats:sup></jats:italic> mice were crossed with the floxed <jats:italic>Sall1</jats:italic> allele, tamoxifen administration during gestation led to a significant decrease in Sall1 expression and small kidneys at birth, suggesting that <jats:italic>Sall1</jats:italic> functions were disrupted. Furthermore, Sall1 expression in the kidney was significantly reduced by neonatal tamoxifen treatment. The <jats:italic>Sall1CreER<jats:sup>T2</jats:sup></jats:italic> mouse is a valuable tool for in vivo time‐dependent and region‐specific knockout and overexpression studies. genesis 48:207–212, 2010. © 2010 Wiley‐Liss, Inc.</jats:p> A mouse line expressing <i>Sall1</i>‐driven inducible Cre recombinase in the kidney mesenchyme genesis |
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| title |
A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme |
| title_unstemmed |
A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme |
| title_full |
A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme |
| title_fullStr |
A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme |
| title_full_unstemmed |
A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme |
| title_short |
A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme |
| title_sort |
a mouse line expressing <i>sall1</i>‐driven inducible cre recombinase in the kidney mesenchyme |
| topic |
Cell Biology Endocrinology Genetics |
| url |
http://dx.doi.org/10.1002/dvg.20603 |
| publishDate |
2010 |
| physical |
207-212 |
| description |
<jats:title>Abstract</jats:title><jats:p><jats:italic>Sall1</jats:italic> is expressed in the metanephric mesenchyme in the developing kidney, and mice deficient in <jats:italic>Sall1</jats:italic> show kidney agenesis or dysgenesis. <jats:italic>Sall1</jats:italic> is also expressed elsewhere, including in the limb buds, anus, heart, and central nervous system. Dominant‐negative mutations of <jats:italic>Sall1</jats:italic> in mice and humans lead to developmental defects in these organs. Here, we generated a mouse line expressing tamoxifen‐inducible Cre recombinase (<jats:italic>CreER<jats:sup>T2</jats:sup></jats:italic>) under the control of the endogenous Sall1 promoter. Upon tamoxifen treatment, these mice showed genomic recombination in the tissues where endogenous <jats:italic>Sall1</jats:italic> is expressed. When <jats:italic>CreER<jats:sup>T2</jats:sup></jats:italic> mice were crossed with the floxed <jats:italic>Sall1</jats:italic> allele, tamoxifen administration during gestation led to a significant decrease in Sall1 expression and small kidneys at birth, suggesting that <jats:italic>Sall1</jats:italic> functions were disrupted. Furthermore, Sall1 expression in the kidney was significantly reduced by neonatal tamoxifen treatment. The <jats:italic>Sall1CreER<jats:sup>T2</jats:sup></jats:italic> mouse is a valuable tool for in vivo time‐dependent and region‐specific knockout and overexpression studies. genesis 48:207–212, 2010. © 2010 Wiley‐Liss, Inc.</jats:p> |
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| author | Inoue, Shuji, Inoue, Miki, Fujimura, Sayoko, Nishinakamura, Ryuichi |
| author_facet | Inoue, Shuji, Inoue, Miki, Fujimura, Sayoko, Nishinakamura, Ryuichi, Inoue, Shuji, Inoue, Miki, Fujimura, Sayoko, Nishinakamura, Ryuichi |
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| description | <jats:title>Abstract</jats:title><jats:p><jats:italic>Sall1</jats:italic> is expressed in the metanephric mesenchyme in the developing kidney, and mice deficient in <jats:italic>Sall1</jats:italic> show kidney agenesis or dysgenesis. <jats:italic>Sall1</jats:italic> is also expressed elsewhere, including in the limb buds, anus, heart, and central nervous system. Dominant‐negative mutations of <jats:italic>Sall1</jats:italic> in mice and humans lead to developmental defects in these organs. Here, we generated a mouse line expressing tamoxifen‐inducible Cre recombinase (<jats:italic>CreER<jats:sup>T2</jats:sup></jats:italic>) under the control of the endogenous Sall1 promoter. Upon tamoxifen treatment, these mice showed genomic recombination in the tissues where endogenous <jats:italic>Sall1</jats:italic> is expressed. When <jats:italic>CreER<jats:sup>T2</jats:sup></jats:italic> mice were crossed with the floxed <jats:italic>Sall1</jats:italic> allele, tamoxifen administration during gestation led to a significant decrease in Sall1 expression and small kidneys at birth, suggesting that <jats:italic>Sall1</jats:italic> functions were disrupted. Furthermore, Sall1 expression in the kidney was significantly reduced by neonatal tamoxifen treatment. The <jats:italic>Sall1CreER<jats:sup>T2</jats:sup></jats:italic> mouse is a valuable tool for in vivo time‐dependent and region‐specific knockout and overexpression studies. genesis 48:207–212, 2010. © 2010 Wiley‐Liss, Inc.</jats:p> |
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| spelling | Inoue, Shuji Inoue, Miki Fujimura, Sayoko Nishinakamura, Ryuichi 1526-954X 1526-968X Wiley Cell Biology Endocrinology Genetics http://dx.doi.org/10.1002/dvg.20603 <jats:title>Abstract</jats:title><jats:p><jats:italic>Sall1</jats:italic> is expressed in the metanephric mesenchyme in the developing kidney, and mice deficient in <jats:italic>Sall1</jats:italic> show kidney agenesis or dysgenesis. <jats:italic>Sall1</jats:italic> is also expressed elsewhere, including in the limb buds, anus, heart, and central nervous system. Dominant‐negative mutations of <jats:italic>Sall1</jats:italic> in mice and humans lead to developmental defects in these organs. Here, we generated a mouse line expressing tamoxifen‐inducible Cre recombinase (<jats:italic>CreER<jats:sup>T2</jats:sup></jats:italic>) under the control of the endogenous Sall1 promoter. Upon tamoxifen treatment, these mice showed genomic recombination in the tissues where endogenous <jats:italic>Sall1</jats:italic> is expressed. When <jats:italic>CreER<jats:sup>T2</jats:sup></jats:italic> mice were crossed with the floxed <jats:italic>Sall1</jats:italic> allele, tamoxifen administration during gestation led to a significant decrease in Sall1 expression and small kidneys at birth, suggesting that <jats:italic>Sall1</jats:italic> functions were disrupted. Furthermore, Sall1 expression in the kidney was significantly reduced by neonatal tamoxifen treatment. The <jats:italic>Sall1CreER<jats:sup>T2</jats:sup></jats:italic> mouse is a valuable tool for in vivo time‐dependent and region‐specific knockout and overexpression studies. genesis 48:207–212, 2010. © 2010 Wiley‐Liss, Inc.</jats:p> A mouse line expressing <i>Sall1</i>‐driven inducible Cre recombinase in the kidney mesenchyme genesis |
| spellingShingle | Inoue, Shuji, Inoue, Miki, Fujimura, Sayoko, Nishinakamura, Ryuichi, genesis, A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme, Cell Biology, Endocrinology, Genetics |
| title | A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme |
| title_full | A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme |
| title_fullStr | A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme |
| title_full_unstemmed | A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme |
| title_short | A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme |
| title_sort | a mouse line expressing <i>sall1</i>‐driven inducible cre recombinase in the kidney mesenchyme |
| title_unstemmed | A mouse line expressing Sall1‐driven inducible Cre recombinase in the kidney mesenchyme |
| topic | Cell Biology, Endocrinology, Genetics |
| url | http://dx.doi.org/10.1002/dvg.20603 |