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Originally published as MBC in Press, 10.1091/mbc.E06-04-0283 on November 8, 2006

Vol. 18, Issue 1, 201-210, January 2007

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Modulation of Gene Expression and Cytoskeletal Dynamics by the Amyloid Precursor Protein Intracellular Domain (AICD)Formula

Thorsten Müller*,{dagger}, Caoimhin G. Concannon{ddagger}, Manus W. Ward{ddagger}, Ciara M. Walsh{ddagger}, Anca L. Tirniceriu*,§, Florian Tribl{dagger}, Donat Kögel||, Jochen H.M. Prehn{ddagger},¶, and Rupert Egensperger*,¶

*Institute of Pathology and Neuropathology, University Hospital Essen, D-45122 Essen, Germany; {ddagger}Department of Physiology and Medical Physics and RCSI Neuroscience Research Centre, Royal College of Surgeons in Ireland, Dublin 2, Ireland; ||Experimental Neurosurgery, Center for Neurology and Neurosurgery, Johann Wolfgang Goethe University Clinics Frankfurt, D-60590 Frankfurt, Germany; {dagger}Medical Proteome-Center, Ruhr-University Bochum, D-44780 Bochum, Germany; and §Institute of Neuropathology, University Hospital Muenster, D-48149 Muenster, Germany

Submitted April 7, 2006; Revised August 14, 2006; Accepted October 26, 2006
Monitoring Editor: Paul Forscher

Amyloidogenic processing of the amyloid precursor protein (APP) results in the generation of beta-amyloid, the main constituent of Alzheimer plaques, and the APP intracellular domain (AICD). Recently, it has been demonstrated that AICD has transactivation potential; however, the targets of AICD-dependent gene regulation and hence the physiological role of AICD remain largely unknown. We analyzed transcriptome changes during AICD-dependent gene regulation by using a human neural cell culture system inducible for expression of AICD, its coactivator FE65, or the combination of both. Induction of AICD was associated with increased expression of genes with known function in the organization and dynamics of the actin cytoskeleton, including {alpha}2-Actin and Transgelin (SM22). AICD target genes were also found to be differentially regulated in the frontal cortex of Alzheimer's disease patients compared with controls as well as in AICD/FE65 transiently transfected murine cortical neurons. Confocal image analysis of neural cells and cortical neurons expressing both AICD and FE65 confirmed pronounced changes in the organization of the actin cytoskeleton, including the destabilization of actin fibers and clumping of actin at the sites of cellular outgrowth. Our data point to a role of AICD in developmental and injury-related cytoskeletal dynamics in the nervous system.

Formula The online version of this article contains supplemental material at MBC Online (http://www.molbiolcell.org).

This article was published online ahead of print in MBC in Press (http://www.molbiolcell.org/cgi/doi/10.1091/mbc.E06-04-0283) on November 8, 2006.

These authors contributed equally to this work.

Address correspondence to: Thorsten Müller (thorsten.t.mueller{at}rub.de)




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