Importin-11 is essential for normal embryonic development in mice

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Title
Importin-11 is essential for normal embryonic development in mice
Author(s)
Ju-Young Lee; R U Rahman; Eun-kyeong KimSang Mi ChoHae-rim KimKihoon LeeChin Soo LeeWoon Kee YoonOg Sung MoonYoung Won SeoYoung Suk WonHyoung-Chin Kim; B H Kim; Ki Hoan Nam
Bibliographic Citation
International Journal of Medical Sciences, vol. 17, no. 6, pp. 815-823
Publication Year
2020
Abstract
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.
Keyword
Importin-11embryonic developmentembryonic lethalknockoutnull mutationphenotype
ISSN
1449-1907
Publisher
Ivyspring Int Publ
DOI
http://dx.doi.org/10.7150/ijms.40697
Type
Article
Appears in Collections:
Ochang Branch Institute > Division of Bioinfrastructure > Laboratory Animal Resource Center > 1. Journal Articles
Ochang Branch Institute > Division of Bioinfrastructure > 1. Journal Articles
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