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Differential Expression of Activator Protein-1 Proteins in the Pineal Gland of Syrian Hamster and Rat May Explain Species Diversity in Arylalkylamine N-Acetyltransferase Gene Expression

Institut des Neurosciences Cellulaires et Intégratives, Département de Neurobiologie des Rythmes, Unité Mixte de Recherche-7168/LC2 Centre National de la Recherche Scientifique-Université Louis Pasteur, Insitut Fédératif de Recherche des Neurosciences de Strasbourg, 67084 Strasbourg, France

Address all correspondence and requests for reprints to: Valérie Simonneaux, Institut des Neurosciences Cellulaires et Intégratives, Département de Neurobiologie des Rythmes, UMR-7168/LC2 CNRS-Université Louis Pasteur, 5 rue Blaise Pascal, 67084 Strasbourg Cedex, France. E-mail: simonneaux{at}neurochem.u-strasbg.fr.

Species differences have been reported for the nighttime regulation of arylalkylamine N-acetyltransferase (AA-NAT), the melatonin rhythm-generating enzyme. In particular, de novo synthesis of stimulatory transcription factors is required for Aa-nat transcription in the Syrian hamster but not in the rat pineal gland. The present work investigated the contribution of phosphorylated cAMP-responsive element-binding protein, c-FOS, c-JUN, and JUN-B in the regulation of Aa-nat transcription in Syrian hamsters compared with rats. The nighttime pattern of cAMP-responsive element-binding protein phosphorylation and regulation by norepinephrine observed in the Syrian hamster was similar to those reported in the rat. On the contrary, strong divergences in c-FOS, c-JUN, and JUN-B expression were observed between both species. In Syrian hamster, predominant expression of c-FOS and c-JUN was observed at the beginning of night, whereas a predominant expression of c-JUN and JUN-B was observed in the late night in rat. The early peak of c-FOS and c-JUN, known to form a stimulatory transcription dimer, suggests that they are involved in the nighttime stimulation of Aa-nat transcription. Indeed, early-night administration of a protein synthesis inhibitor (cycloheximide) markedly decreased AA-NAT mRNA levels in Syrian hamster. In the rat, high levels of JUN-B and c-JUN, constituting an inhibitory transcription dimer, are probably involved in the late-night inhibition of Aa-nat transcription. Early-night administration of cycloheximide actually increased AA-NAT mRNA levels toward the late night. Therefore, composition and timing of the pineal activator protein-1 complexes differ between rat and Syrian hamster and may be an activator (Syrian hamster) or an inhibitor (rat) of Aa-nat transcription.

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