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Targeted disruption of the mouse Asna1 gene results in embryonic lethality
Author(s) -
Mukhopadhyay Rita,
Ho Ye-Shih,
Swiatek Pamela J.,
Rosen Barry P.,
Bhattacharjee Hiranmoy
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.06.017
Subject(s) - gene knockout , embryonic stem cell , knockout mouse , biology , phenotype , embryo , atpase , homologous recombination , gene , homologous chromosome , lethality , microbiology and biotechnology , wild type , embryogenesis , mutant , genetics , biochemistry , enzyme
The bacterial ArsA ATPase is the catalytic component of an oxyanion pump that is responsible for resistance to arsenicals and antimonials. Homologues of the bacterial ArsA ATPase are widespread in nature. We had earlier identified the mouse homologue (Asna1) that exhibits 27% identity to the bacterial ArsA ATPase. To identify the physiological role of the protein, heterozygous Asna1 knockout mice ( Asna1 +/− ) were generated by homologous recombination. The Asna1 +/− mice displayed similar phenotype as the wild‐type mice. However, early embryonic lethality was observed in homozygous Asna1 knockout embryos, between E3.5 (E = embryonic day) and E8.5 stage. These findings indicate that Asna1 plays a crucial role during early embryonic development.