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Development ePress online publication date 1 Jun 2005
doi: 10.1242/dev.01864

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Research article

Essential role of protein kinase B{gamma} (PKB{gamma}/Akt3) in postnatal brain development but not in glucose homeostasis


Oliver Tschopp, Zhong-Zhou Yang, Daniela Brodbeck, Bettina A. Dummler, Maja Hemmings-Mieszczak, Takashi Watanabe, Thomas Michaelis, Jens Frahm, and Brian A. Hemmings*
* Author for correspondence (e-mail: brian.hemmings{at}fmi.ch)

Protein kinase B is implicated in many crucial cellular processes, such as metabolism, apoptosis and cell proliferation. In contrast to Pkb{alpha} and Pkb{beta}-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.


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