Restricted expression and photic induction of a novel mouse regulatory factor X4 transcript in the suprachiasmatic nucleus.

The regulatory factor X (RFX) family of transcription factors is characterized by a unique and highly conserved 76-amino acid residue DNA-binding domain. Mammals have five RFX genes, but the physiological functions of their products are unknown, with the exception of RFX5.Here a mouse RFX4 transcript was identified that encodes a peptide of 735 amino acids, including the DNA-binding domain. Its expression was localized in the suprachiasmatic nucleus, the central pacemaker site of the circadian clock. Also, light exposure was found to induce its gene expression in a subjective night-specific manner. Polyclonal antibodies were prepared, and an 80-kDa band was detected in the suprachiasmatic nucleus by Western hybridization. A histochemical study showed a localization of the products in the nucleus. This is the first report on mouse RFX4, which contains the RFX DNA-binding motif. Our investigation may provide clues to the physiological function of RFX4

Identification of genes that express in response to light exposure and express rhythmically in a circadian manner in the mouse suprachiasmatic nucleus

Most biological phenomena,including behavoir and metabolic pathways,are governed by an internal clock system that is circadian (i.e.,with a period of approximately 24 h) and is reset by light exposure from outside.In order to understand the molecular basis of the resetting mechanism of the clock,we attempted to isolate light-inducible transcripts in the suprachiasmatic nucleus,where the master clock resides,using a new gene expression profiling procedure.We identified 87 such transcripts,successfully cloned 60 of them and 17 are protein-coding transcripts registered in the public database that were not known to be light inducible.Induction is subjective night specific in most of the transcripts.Interestingly,6 of the transcripts exhibit rhythmic expression in a circadian manner in the suprachiasmatic nucleus

Mouse dexamethasone-induced RAS protein 1 gene is expressed in a circadian rhythmic manner in the suprachiasmatic nucleus.

We identified the Dexamethasone-induced RAS protein 1 (Dexras1) gene as a cycling gene in the suprachiasmatic nucleus (SCN). Investigation of the whole brain using in situ hybridization demonstrated the localization of the expression of the gene in the SCN, thalamus, piriform cortex and hippocampus. However, rhythmic expression of the gene was observed only in the SCN. The rhythmic change in gene expression during 1 day was approximately five-fold, and the maximum expression was observed during subjective night. Real-time PCR using the SCN, paraventricular nucleus and cortex confirmed these results. Next, we analyzed the expression of the Dexras1 gene in the SCN of cryptochrome (Cry) 1 and 2 double knockout mice. We found that the rhythmic expression disappeared. The results indicate that Dexras1 rhythmicity and levels are dependent upon CRYs. This is the first time that the G protein, which may be involved in the input pathway, has been isolated as a cycling gene in the SCN.\nMouse dexamethasone-induced RAS protein 1 gene is expressed in a circadian rhythmic manner in the suprachiasmatic nucleus.\nTakahashi H, Umeda N, Tsutsumi Y, Fukumura R, Ohkaze H, Sujino M, van der Horst G, Yasui A, Inouye ST, Fujimori A, Ohhata T, Araki R, Abe M.\nTranscriptome Profiling Group, National Institute of Radiological Sciences, Anagawa 4-9-1, Inage-ku, Chiba 263-8555, Japan.\nWe identified the Dexamethasone-induced RAS protein 1 (Dexras1) gene as a cycling gene in the suprachiasmatic nucleus (SCN). Investigation of the whole brain using in situ hybridization demonstrated the localization of the expression of the gene in the SCN, thalamus, piriform cortex and hippocampus. However, rhythmic expression of the gene was observed only in the SCN. The rhythmic change in gene expression during 1 day was approximately five-fold, and the maximum expression was observed during subjective night. Real-time PCR using the SCN, paraventricular nucleus and cortex confirmed these results. Next, we analyzed the expression of the Dexras1 gene in the SCN of cryptochrome (Cry) 1 and 2 double knockout mice. We found that the rhythmic expression disappeared. The results indicate that Dexras1 rhythmicity and levels are dependent upon CRYs. This is the first time that the G protein, which may be involved in the input pathway, has been isolated as a cycling gene in the SCN

〈Originals〉Profile of tyrosine hydroxylase-expressing neurons in the olfactory bulb of prokineticin type 2 receptor-deficient mice during embryonic development

[Abstract]　Dopamine neurons in the olfactory bulb play essential roles in the maintenance of olfactory function. The maturation of these neurons involves mitosis, cell migration and the transcriptional regulation of specific neurotransmitters and is an intensively studied process. In our present study, we investigated the embryonic development of tyrosine-hydroxylase (TH)-expressing neurons in the main olfactory bulb (MOB) of Pkr2^ mice that lack axonal infiltration from the olfactory neurons (ON) and wild-type littermates (WT) at E16.5, E18.5 and P0 using immunohistochemical techniques. Even at E16.5, we observed two populations of neurons in the MOB of WT mice, one scattered in the primitive glomerular layer and another population of TH-positive neurons in the surface region of the primitive granular cell layer. The number of TH-positive neurons had increased markedly by P0. Pkr2^ mouse embryos and neonates showed disorganization of the layered structure, mainly due to the loss of glomerular layer in the olfactory system. The number of TH-immunoreactive cells per slice was markedly lower at P0 but not at E16.5 and E18.5. Interestingly, even in Pkr2^ mice, TH-immunoreactive neurons were still present in the periphery of the MOB. Hence, it is highly probable that the lack of Pkr2-i- does not affect the migration of TH-containing neurons from the subventricular zone to the periphery of the MOB during embryonic development but strongly impairs the migration of TH-expressing neurons or TH expression in the MOB around birth.Masumoto, Koh-he