Invited review c-Fos as a transcription factor: a stressful (re)view from a functional map
Section snippets
Introductioncm
Stereotypic inducibility of c-fos proto-oncogene rendered this cellular immediate-early gene (IEG) to be the most widely used functional anatomical mapping tool to identify cells and extended circuitries that became activated in response to various stimuli (Greenberg and Ziff, 1984;Sagar et al., 1988; Ceccatelli et al., 1989; Bullit, 1990). On the other hand, c-fos (and other members of its family) by dimerization with that of the members of the jun family, forms a transcription factor referred
c-fos and their relatives
To date four major protein members of the Fos family have been identified: c-Fos, FosB, Fra-1 and Fra-2. (Greenberg and Ziff, 1984; Zerial et al.; 1989; Cohen and Curran, 1988; Nishina et al.; 1990) (see Table 1). These proteins are encoded by genes containing four exons and three introns (van Straaten et al., 1983) and possess a leucin zipper motif that promotes heterodimerization with that of the members of the Jun family (c-jun, JunB and JunD) to form a transcription factor referred to as
c-fos induction in the paraventricular nucleus
One of the best output of the c-fos strategy is the functional anatomical mapping of neuronal circuits underlying neuronendocrine-, autonomical- and behavioral responses induced by stress. Exogenous and endogenous challenges activate the parvocellular neurosecretory neurons in the hypothalamic paraventricular nucleus to initiate stress cascade by delivering the two main corticotropin releasing factors, CRF-41 and arginine vasopressin into the hypophyseal portal circulation (review: see Antoni,
Summary
c-fos-based functional mapping has been validated as a powerful technic to reveal activated neurons and characterize cell groups that may be associated with functional circuits in a situation specific manner, in spite of uncertainties the exact functional roles of c-Fos, as a transcription factor, in the central nervous system as well as about the signal transduction mechanisms that activate immediate-early gene induction in vivo.
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