Int J Med Sci 2020; 17(6):815-823. doi:10.7150/ijms.40697 This issue
1. Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Yeonjudanji-ro 30, Chungbuk 28116, Korea.
2. Department of Public Health, College of Natural Science, Keimyung University, Daegu, 42601, Korea.
*These authors are contributed equally to this study.
Importin-11 (Ipo11) is a novel member of the human importin family of transport receptors (karyopherins), which are known to mediate the nucleocytoplasmic transport of protein and RNA cargos. Despite its role in the transport of protein, we found that knockout of Ipo11 nuclear import factor affects normal embryonic development and govern embryo-lethal phenotypes in mice. In this study, we for the first time produced a mouse line containing null mutation in Ipo11 gene utilized by gene trapping. The Ipo11-/- embryos showed an embryonic lethal phenotype. The Ipo11-/- embryos showed a reduced size at embryonic day 10.5 (E10.5) when compared with Ipo11+/+ or Ipo11+/- embryos and died by E11.5. Whereas Ipo11+/- mice were healthy and fertile, and there was no detectable changes in embryonic lethality and phenotype when reviewed. In the X-gal staining with the Ipo11-/- or Ipo11+/- embryos, strong X-gal staining positivity was detected systematically in the whole mount embryos at E10.5, although almost no X-gal positivity was detected at E9.5, indicating that the embryos die soon after the process of Ipo11 expression started. These results indicate that Ipo11 is essential for the normal embryonic development in mice.
Keywords: Importin-11, embryonic lethal, null mutation, knockout, embryonic development, phenotype