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C-H Lee, L Chang, and L-N Wei


An alternatively spliced variant of a testis-specific nuclear orphan receptor TR2-11 was identified and designated as TR2-11-t. As a result of retaining intron 5 of this gene, TR2-11-t mRNA encoded a truncated receptor with the complete ligand-binding domain deleted. Protein expression of both isoforms was confirmed using a prokaryotic expression system. In the mouse, the expression of the two TR2 isoforms was elevated in the testis with distinct profiles beginning at puberty. TR2-11 expression increased at postnatal day 18, peaked between day 20 and day 24 and remained at high levels throughout adulthood, whereas TR2-11-t expression was elevated transiently at postnatal day 24. Among separated primary germ cells and established testicular cell lines, TR2-11 was expressed highly in meiotic and postmeiotic germ cells and weakly in a Leydig cell line and a germ cell line, but not expressed in a Sertoli cell line. In contrast, TR2-11-t was expressed at a much lower level in all the testicular cell types examined. In adult testes blocked at germ cell development by vitamin A depletion or hypophysectomy, TR2-11 expression was dramatically reduced whereas TR2-11-t was highly elevated. Based upon the RNA expression patterns of these isoforms, it was suggested that TR2-11 was specific to meiotic and postmeiotic germ cells whereas TR2-11-t was enriched in early germ cell populations such as premeiotic cells. The biological activities of TR2-11 and TR2-11-t on a direct repeat 5-type retinoic acid (RA) response element (RARE)-containing reporter gene was examined in Cos cells. TR2-11 repressed RA induction of this reporter whereas TR2-11-t enhanced RA induction of the same reporter, and the opposite biological effects of these isoforms were dose-dependent. Gel-shift experiments provided evidence for a direct interaction of TR2-11, but not TR2-11-t, with DNA fragments containing this RARE. Opposite roles of TR2-11 and TR2-11-t on RA induction of promoters containing this particular RARE are suggested.

Journal of Endocrinology (1997) 152, 245–255

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Y Yang, J Cao, W Xiong, J Zhang, Q Zhou, H Wei, C Liang, J Deng, T Li, S Yang, and L Xu

It has been documented that stress or glucocorticoids have conflicting effects on memory under different conditions. However, it is not fully understood why stress can either impair or enhance memory. Here, we have examined the performance of six age groups of Wistar rats in a water maze spatial task to evaluate the effects of stress under different conditions. We found that the impairment or enhancement effect of an 'elevated platform' (EP) stress on memory was dependent on previous stress experience and on age. EP stress impaired memory retrieval in water maze naive animals, but enhanced rather than impaired memory retrieval in young water maze stress-experienced animals. Furthermore, exogenously applied corticosterone or foot shock stress before water maze training prevented the impairment of memory retrieval that should be induced by treatment with corticosterone or foot shock before the 'probe trial'. Again, memory retrieval was enhanced in young animals under these conditions, and this enhancement can be prevented by the glucocorticoid receptor antagonist RU 38486. Thus, glucocorticoid receptor activation not only induced impairment of memory but also increased the capacity of young animals to overcome a later stress. The present findings suggest that the effect of stress on memory can be switched from impairment to enhancement dependent on both stress experience and age.

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S Wei, Y Feng, FY Che, H Pan, N Mzhavia, LA Devi, AA McKinzie, N Levin, WG Richards, and LD Fricker

ProSAAS is a neuroendocrine peptide precursor that potently inhibits prohormone convertase 1 in vitro. To explore the function of proSAAS and its derived peptides, transgenic mice were created which express proSAAS using the beta-actin promoter. The body weight of transgenic mice was normal until approximately 10-12 weeks, and then increased 30-50% over wild-type littermates. Adult transgenic mice had a fat mass approximately twice that of wild-type mice, and fasting blood glucose levels were slightly elevated. In the pituitary, the levels of several fully processed peptides in transgenic mice were not reduced compared with wild-type mice, indicating that the proSAAS transgene did not affect prohormone convertase 1 activity in this tissue. Because the inhibitory potency of proSAAS-derived peptides towards prohormone convertase 1 is much greater in the absence of carboxypeptidase E activity, the proSAAS transgene was also expressed in carboxypeptidase E-deficient Cpe (fat/fat) mice. Although the transgenic mice were born in the expected frequency, 21 of 22 proSAAS transgenic Cpe (fat/fat) mice died between 11 and 26 weeks of age, presumably due to greatly elevated blood glucose. The levels of several pituitary peptides were significantly reduced in the proSAAS transgenic Cpe (fat/fat) mice relative to non-transgenic Cpe (fat/fat) mice, suggesting that the transgene inhibited prohormone convertase 1 in these mice. Taken together, these results are consistent with a role for proSAAS-derived peptides as neuropeptides that influence body weight independently of their function as inhibitors of prohormone convertase 1.