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A more recent version of this article appeared on April 1, 2004
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Submitted on September 30, 2003
Revised on December 23, 2003
Accepted on January 10, 2004
1 CIQUIBIC (CONICET), Departamento de Química Biológica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina
* Corresponding author. E-mail address: bcaputto{at}dqbfcq.uncor.edu.
We have shown that c-Fos activates phospholipid synthesis through a mechanism independent of its genomic AP-1 activity (FASEB Journal, 2001. 15:556-558. First published on January 5, 2001; 10.1096/fj.00-0446fje). Herein, using PC12 cells induced to differentiate by NGF, the genomic effect of c-Fos in initiating neurite outgrowth is shown as distinct from its nongenomic effect of activating phospholipid synthesis and sustaining neurite elongation. Blocking c-Fos expression inhibited differentiation, phospholipid synthesis activation and neuritogenesis. In cells primed to grow, blocking c-Fos expression determined neurite retraction. However, transfected cells expressing c-Fos or c-Fos deletion mutants with capacity to activate phospholipid synthesis, sustain neurite outgrowth and elongation in the absence of NGF. RESULTS disclose a dual function of c-Fos: it first releases the genomic program for differentiation and then associates to the ER and activates phospholipid synthesis. Since phospholipids are key membrane components, we hypothesize this latter phenomenon as crucial to support membrane genesis demands required for cell growth and neurite elongation.
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