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First published online 1 June 2005
doi: 10.1242/dev.01864
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(PKB/Akt3) in postnatal brain development but not in glucose homeostasis
1 Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66,
CH-4058 Basel, Switzerland
2 Novartis Pharma AG, Lichtstrasse 35, CH-4056, Basel, Switzerland
3 Biomedizinische NMR Forschungs GmbH am Max-Planck-Institut für
biophysikalische Chemie, 37070 Göttingen, Germany
* Author for correspondence (e-mail: brian.hemmings{at}fmi.ch)
Accepted 14 April 2005
Protein kinase B is implicated in many crucial cellular processes, such as
metabolism, apoptosis and cell proliferation. In contrast to
Pkb
and Pkbß-deficient mice,
Pkb
-/- mice are viable, show no growth retardation
and display normal glucose metabolism. However, in adult Pkb
mutant mice, brain size and weight are dramatically reduced by about 25%. In
vivo magnetic resonance imaging confirmed the reduction of
Pkb-/- brain volumes with a proportionally smaller
ventricular system. Examination of the major brain structures revealed no
anatomical malformations except for a pronounced thinning of white matter
fibre connections in the corpus callosum. The reduction in brain
weight of Pkb-/- mice is caused, at least
partially, by a significant reduction in both cell size and cell number. Our
results provide novel insights into the physiological role of PKB and
suggest a crucial role in postnatal brain development.
Key words: Pkb/Akt3 knockout, Brain development, Apoptosis
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