C-FOS DEFICIENCY INHIBITS INDUCTION OF MESSENGER-RNA FOR SOME, BUT NOT ALL, NEUROTRANSMITTER BIOSYNTHETIC-ENZYMES BY IMMOBILIZATION STRESS

Recent studies indicated that c-Fos protein may be mediating stress-el icited transcriptional activation of genes involved in neurotransmitte r biosynthesis. However, direct evidence for c-Fos mediating these cha nges in gene expression has been lacking. Mice with disrupted c-fos ge ne(+/- or -/-genotypes) were used to examine the effect of immobilizat ion stress on a group of stress-responsive genes, in male adrenals, c- Fos was found not essential for stress-elicited activation of expressi on of tyrosine hydroxylase, dopamine beta-hydroxylase (DBH), phenyleth anolamine N-methyltransferase, or neuropeptide Y. In females, immobili zation failed to induce adrenal DBH in the c-fos-deficient mice. In br ainstem, c-Fos was indispensable for elevation of DBH mRNA in both gen ders. The gene, gender, and tissue specificity in the requirement for G-Fos points to diversity in adaptation mechanisms to stress.