SynaptogenesisRegulatesAxotomy-InducedActivationof c-Jun-ActivatorProtein-1Transcription

Axotomy initiates changes in gene expression that either resultsin programmed cell death or promotes and sustains axon growthand other concomitants of regeneration. Once contact with atarget has been reestablished, regeneration-specific transcriptionis generally downregulated to a basal state (Ambron and Walters,1996). These alterations, in response to events in the periphery,require complex signaling cascades to the nucleus and preciselyintegrated control of specific transcription factors (Ambron andWalters, 1996; Tanaka et al., 1998; Sung et al., 2001; Zimmer-mann, 2001). To begin to understand how injury and target-derivedsignalsregulatetranscription,weexaminedthewellchar-acterized activator protein-1 (AP1) transcription complexcomprising the Fos/activating transcription factor (ATF) and theJunsubfamiliesofbasic-regionleucine-zipperproteins(Shaulianand Karin, 2002). These factors form homodimeric or het-erodimeric complexes that bind to 12–0-tetradecanoyl-phorbol-13-acetate (TPA) response element (TRE) or cAMP response el-ement (CRE) consensus sequences (Herdegen and Leah, 1998;Chinenov and Kerppola, 2001). Dimer formation, DNA binding,and the ability to