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Molecular and Cellular Biology, January 2004, p. 294-305, Vol. 24, No. 1
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.1.294-305.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Mice Deficient for the Ets Transcription Factor Elk-1 Show Normal Immune Responses and Mildly Impaired Neuronal Gene Activation

Francesca Cesari,1 Stephan Brecht,2 Kristina Vintersten,3,{dagger} Lam Giang Vuong,1 Matthias Hofmann,4,{ddagger} Karin Klingel,5 Jens-Jörg Schnorr,5,§ Sergei Arsenian,1 Hansjörg Schild,4 Thomas Herdegen,2 Franziska F. Wiebel,1 and Alfred Nordheim1*

Abteilung Molekularbiologie,1 Abteilung Immunologie, Interfakultäres Institut für Zellbiologie, Universität Tübingen,4 Abteilung für Molekulare Pathologie, Universitätsklinikum Tübingen, Tübingen,5 Institut für Pharmakologie, Universitätsklinikum Schleswig-Holstein, Kiel,2 European Molecular Biology Laboratories, Heidelberg, Germany3

Received 9 June 2003/ Returned for modification 5 August 2003/ Accepted 25 August 2003

The transcription factor Elk-1 belongs to the ternary complex factor (TCF) subfamily of Ets proteins. TCFs interact with serum response factor to bind jointly to serum response elements in the promoters of immediate-early genes (IEGs). TCFs mediate the rapid transcriptional response of IEGs to various extracellular stimuli which activate mitogen-activated protein kinase signaling. To investigate physiological functions of Elk-1 in vivo, we generated Elk-1-deficient mice by homologous recombination in embryonic stem cells. These animals were found to be phenotypically indistinguishable from their wild-type littermates. Histological analysis of various tissues failed to reveal any differences between Elk-1 mutant and wild-type mice. Elk-1 deficiency caused no changes in the proteomic displays of brain or spleen extracts. Also, no immunological defects could be detected in mice lacking Elk-1, even upon infection with coxsackievirus B3. In mouse embryonic fibroblasts, Elk-1 was dispensable for c-fos and Egr-1 transcriptional activation upon stimulation with serum, lysophosphatidic acid, or tetradecanoyl phorbol acetate. However, in brains of Elk-1-deficient mice, cortical and hippocampal CA1 expression of c-fos, but not Egr-1 or c-Jun, was markedly reduced 4 h following kainate-induced seizures. This was not accompanied by altered patterns of neuronal apoptosis. Collectively, our data indicate that Elk-1 is essential neither for mouse development nor for adult life, suggesting compensatory activities by other TCFs.

* Corresponding author. Mailing address: Universität Tübingen, Auf der Morgenstelle 15, 72076 Tübingen, Germany. Phone: 49-70701-297 8898. Fax: 49-7071-29 53 59. E-mail: alfred.nordheim{at}uni-tuebingen.de.

{dagger} Present address: Mount Sinai Hospital, Samuel Lunenfeld Research Institute, Toronto, Canada.

{ddagger} Present address: Novartis Pharma AG, Transplantation Research, Basel, Switzerland.

§ Present address: Deutsches Zentrum für Luft- und Raumfahrt, Bonn, Germany.

Molecular and Cellular Biology, January 2004, p. 294-305, Vol. 24, No. 1
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.1.294-305.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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