Generation of cortactin floxed mice and cellular analysis of motility in fibroblasts |
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| Authors: | Shinji Tanaka Masataka Kunii Akihiro Harada Shigeo Okabe |
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| Affiliation: | 1. Department of Cellular Neurobiology, Graduate School of Medicine, The University of Tokyo, 7‐3‐1 Hongo Bunkyo‐ku, Tokyo, Japan;2. Department of Cell Biology, School of Medicine, Tokyo Medical and Dental University, 1‐5‐45 Yushima, Bunkyo‐ku, Tokyo, Japan;3. Laboratory of Molecular Traffic, Department of Molecular and Cellular Biology, Institute for Molecular and Cellular Regulation, Gunma University, 3‐39‐15 Showa, Maebashi, Gunma, Japan;4. Department of Cell Biology, Graduate School of Medicine, Osaka University, 2‐2 Yamadaoka, Suita, Osaka, Japan |
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| Abstract: | Cortactin is an F‐actin binding protein that has been suggested to play key roles in various cellular functions. Here, we generated mice carrying floxed alleles of the cortactin (Cttn) gene (Cttnflox/flox mice). Expression of Cre recombinase in mouse embryonic fibroblasts (MEFs) isolated from Cttnflox/flox embryos depleted cortactin within days, without disturbing F‐actin distribution and localization of multiple actin‐binding proteins. Cre‐mediated deletion of Cttn also did not affect cell migration. To obtain mice with a Cttn null allele, we next crossed Cttnflox/flox mice with transgenic mice that express Cre recombinase ubiquitously. Western blot and immunocytochemical analysis confirmed complete elimination of cortactin expression in MEFs carrying homozygously Cttn null alleles. However, we found no marked alteration of F‐actin organization and cell migration in Cttn null‐MEFs. Thus, our results indicate that depletion of cortactin in MEFs does not profoundly influence actin‐dependent cell motility. genesis 47:638–646, 2009. © 2009 Wiley‐Liss, Inc. |
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| Keywords: | cortactin actin filament conditional knockout mouse embryonic fibroblasts cell migration |
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