Targeted disruption of the mouse Asna1 gene results in embryonic lethality

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 bacteri...

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Bibliographic Details
Published in:FEBS letters 2006-07, Vol.580 (16), p.3889-3894
Main Authors: Mukhopadhyay, Rita, Ho, Ye-Shih, Swiatek, Pamela J., Rosen, Barry P., Bhattacharjee, Hiranmoy
Format: Article
Language:English
Subjects:
Animals
ArsA
Arsenic
Arsenite Transporting ATPases
Asna1
Embryo Loss - genetics
Embryonic lethality
Exons - genetics
Gene Expression Profiling
Gene Targeting
Genotype
Ion Pumps - deficiency
Ion Pumps - genetics
Knockout mouse
Mice
Multienzyme Complexes - deficiency
Multienzyme Complexes - genetics
Phenotype
Recombination, Genetic - genetics
RNA, Messenger - genetics
RNA, Messenger - metabolism
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Summary: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.
ISSN:0014-5793
1873-3468
DOI:10.1016/j.febslet.2006.06.017