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First published online 1 June 2005
doi: 10.1242/dev.01864

Development 132, 2943-2954 (2005)
Published by The Company of Biologists 2005
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Essential role of protein kinase B{gamma} (PKB{gamma}/Akt3) in postnatal brain development but not in glucose homeostasis

Oliver Tschopp1, Zhong-Zhou Yang1, Daniela Brodbeck1, Bettina A. Dummler1, Maja Hemmings-Mieszczak2, Takashi Watanabe3, Thomas Michaelis3, Jens Frahm3 and Brian A. Hemmings1,*

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{alpha} and Pkbß-deficient mice, Pkb{gamma}-/- mice are viable, show no growth retardation and display normal glucose metabolism. However, in adult Pkb{gamma} mutant mice, brain size and weight are dramatically reduced by about 25%. In vivo magnetic resonance imaging confirmed the reduction of Pkb{gamma}-/- 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{gamma}-/- 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{gamma} and suggest a crucial role in postnatal brain development.

Key words: Pkb{gamma}/Akt3 knockout, Brain development, Apoptosis






© The Company of Biologists Ltd 2005