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The Journal of Neuroscience, November 15, 1998, 18(22):9192-9203
Na,K-ATPase Subunit  1 knock-in Prevents Lethality
of 2 Deficiency in Mice
Philipp
Weber1,
Udo
Bartsch1,
Melitta
Schachner1, 2, and
Dirk
Montag1, 3
1 Department of Neurobiology, Swiss Federal Institute
of Technology, CH-8093 Zürich, Switzerland, 2 Zentrum
für Molekulare Neurobiologie, Universität Hamburg, D-20246
Hamburg, Germany and 3 Research Group Neurogenetics,
Leibniz Institute for Neurobiology, D-39118 Magdeburg, Germany
The  2 subunit of the Na,K-ATPase displays functional properties
of both an integral constituent of an ion pump and an adhesion and
neurite outgrowth-promoting molecule in vitro. To
investigate whether the 1 subunit of the Na,K-ATPase can
functionally substitute for the 2 isoform in vivo, we
have generated 2/1 knock-in mice by homologous
recombination in embryonic stem cells. In 2/1 knock-in mice, expression of 2 was abolished, whereas
1 mRNA expression from the mutated gene amounted to ~15% of the
normal expression of 2 in the adult mouse brain and prevented the
juvenile lethality observed for 2 null mutant mice. In contrast to
2 null mutant mice, the overall morphological structure of all
analyzed brain regions was normal. By immunohistochemical analysis,
1 expression was detected in photoreceptor cells in the retina of knock-in mice at an age when expression of 1 and
2, respectively, is downregulated and persisting in the wild-type
mice. Morphological analysis by light and electron microscopy revealed
a progressive degeneration of photoreceptor cells. Apoptotic death of
photoreceptor cells determined quantitatively by terminal
deoxynucleotidyl transferase-mediated dUTP nick end labeling analysis
increased in 2/1 knock-in mice with age. These
observations suggest that the 1 subunit of the Na,K-ATPase can
substitute sufficiently, at least in certain cell types, for the role
of the 2 subunit as a component of a functional Na,K-ATPase, but
they do not allow us to determine the possible role of the 2 subunit
as an adhesion molecule in vivo.
Key words:
Na,K-ATPase; knock-in; retinitis pigmentosa; photoreceptor cells; adhesion molecule on glia; AMOG; mouse;
subunit; ionic homeostasis
Copyright © 1998 Society for Neuroscience 0270-6474/98/18229192-12$05.00/0
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