cAMP-response element modulator tau is a positive regulator of testis angiotensin converting enzyme transcription.

Zhou, Yifeng; Sun, Zuoming; Means, Anthony R.; Sassone–Corsi, Paolo; Bernstein, Kenneth E.

doi:10.1073/pnas.93.22.12262

Cited by 75 publications

(48 citation statements)

References 28 publications

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“…The positions from the transcription start site and sequences of oligonucleotides were as follows: Ϫ250/Ϫ216, 5Ј-CAACCATTTGTAGGAATGAACAAAGAGGGAAATAA-3Ј; Ϫ96/Ϫ47, 5Ј-GCCTAAATTGGGATGCTTGCCTTATGAGAAGAAACATTTTAAC-GGAGTGG-3Ј; Ϫ61/Ϫ12, 5Ј-ATTTTAACGGAGTGGTGGGTGGGGTG-GGGCCCTATTTATGACACAAGAGA-3Ј; Ϫ69/Ϫ25(mut Ϫ49/Ϫ36), 5Ј-GAAGAAACATTTTAACGGAGgaattctgttctgtGGGCCCTATTT-3Ј; Ϫ28/ϩ22, 5Ј-ATTTATGACACAAGAGAGCAAGCCCCTCCCTTCTTGT-AAGAGAGTGCTAG-3Ј. 32 P-Labeled DNA (1 ng at ϳ100,000 cpm/ng) was incubated in binding buffer (10 mM HEPES, pH 7.9, 60 mM KCl, 1 mM EDTA, 5 mM DTT, 4 mM spermidine, 5 mM MgCl 2 , 10% glycerol, and 1 g of poly(dI-dC) (Amersham Pharmacia Biotech)) on ice for 30 min with testis (10 g), liver (8 g), and germ cell (10 g) nuclear extracts in a total reaction volume of 25 l. Binding buffer for Ϫ250/Ϫ216 oligonucleotide included 0.5 g of poly(dG-dC) (Amersham Pharmacia Biotech) instead of 1 g of poly(dI-dC). In some experiments with the Ϫ61/Ϫ12 oligonucleotide, ZnCl 2 was added in the binding buffer and 4% Ficoll 400 was used instead of 10% glycerol.…”

Section: Tissue Preparation and Immunohistochemistry-micementioning

confidence: 99%

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Testis Hormone-sensitive Lipase Expression in Spermatids Is Governed by a Short Promoter in Transgenic Mice

Blaise¹,

Guillaudeux²,

Tavernier³

et al. 2001

Journal of Biological Chemistry

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A testicular form of hormone-sensitive lipase (HSL tes ), a triacylglycerol lipase, and cholesterol esterase, is expressed in male germ cells. Northern blot analysis showed HSL tes mRNA expression in early spermatids. Immunolocalization of the protein in human and rodent seminiferous tubules indicated that the highest level of expression occurred in elongated spermatids. We have previously shown that 0.5 kilobase pairs of the human HSL tes promoter directs testis-specific expression of a chloramphenicol acetyltransferase reporter gene in transgenic mice and determined regions binding nuclear proteins expressed in testis but not in liver (Blaise, R., Grober, J., Rouet, P., Tavernier, G., Daegelen, D., and Langin, D. (1999) J. Biol. Chem. 274, 9327-9334). Mutation of a SRY/Sox-binding site in one of the regions did not impair in vivo testis-specific expression of the reporter gene. Further transgenic analyses established that 95 base pairs upstream of the transcription start site were sufficient for correct testis expression. In gel retardation assays using early spermatid nuclear extracts, a germ cell-specific DNA-protein interaction was mapped between ؊46 and ؊29 base pairs. The DNA binding nuclear protein showed properties of zinc finger transcription factors. Mutation of the region abolished reporter gene activity in transgenic mice, showing that it is necessary for testis expression of HSL tes . Hormone-sensitive lipase (HSL)1 hydrolyzes triacylglycerol and, cholesterol and retinyl esters (1, 2). In adipose tissue, HSL catalyzes the rate-limiting step in lipolysis, the catabolic pathway that mobilizes fatty acids from triacylglycerol stored in the lipid droplet. HSL is also expressed in rodent and human testis (3-5). In situ hybridization experiments performed in rat testis showed strong labeling of cells in the adluminal parts of the seminiferous tubules at stages X-XIV and sparsely distributed grains in the basal parts (6). Immunohistochemistry experiments showed an HSL-like immunoreactivity in the adluminal part of the rat seminiferous tubules at stages XIII-VIII (5). The data suggested that rodent HSL mRNA and protein are expressed in haploid germ cells with a lag between mRNA and protein appearance. However, the precise germ cell type(s) expressing HSL was not determined in rat and it was not possible to rule out HSL expression in Sertoli cells. Moreover, the expression of HSL in germ cells of other mammalian species, including man, has not been documented. The effects of HSL gene disruption in mice have recently been reported (7). The most striking feature of the phenotype is male sterility due to oligospermia. Degenerated spermatocytes and spermatids were observed in HSL-deficient testis with a lack of mature spermatozoa. The data clearly demonstrate that HSL is required for spermatogenesis.The human adipose tissue form of HSL is encoded by 9 exons spanning 11 kb (8). The transcription start site was mapped in a short 5Ј-noncoding exon located 1.5 kb upstream of the first coding exon (9). The 2.8-kb mR...

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Section: Tissue Preparation and Immunohistochemistry-micementioning

confidence: 99%

“…A subset of them are under the direct control of cAMP-responsive element modulator , e.g. the angiotensin-converting enzyme and protamine 1 promoters (31,32). Others are activated by cAMP-responsive element modulator -independent mechanisms such as the lactate dehydrogenase c, ␤1,4-galactosyltransferase I, and HSL tes promoters (29,30).…”

Section: Figmentioning

confidence: 99%

Testis Hormone-sensitive Lipase Expression in Spermatids Is Governed by a Short Promoter in Transgenic Mice

Blaise¹,

Guillaudeux²,

Tavernier³

et al. 2001

Journal of Biological Chemistry

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“…This site has been located from Ϫ55 to Ϫ48 relative to the transcriptional start site and has been shown to be a binding site for CREM (17). A small portion of the angiotensin-converting enzyme promoter from Ϫ91 to ϩ17 can efficiently target a reporter construct to step 4 -14 spermatids (38,39).…”

Section: Figmentioning

confidence: 99%

“…Target gene disruption of the CREM gene (including CREM ) leads to infertility in transgenic mice (14,15). Moreover, CRE-binding sites have frequently been observed in testicular expressed genes implicated in spermatogenesis and fertility (8,16,17), suggesting a critical role for CREM in proper regulation of these genes during spermatogenesis.Germ cell nuclear factor (also known as retinoid receptorrelated testis-associated receptor) is a member of the nuclear receptor superfamily of ligand-activated transcription factors (18, 19); however, a ligand for GCNF is currently unknown. Target gene disruption of GCNF leads to embryonic lethality * This work was supported by grants from the Deutsche Forschungsgemeinschaft (GRK336 and WE2458/3-1) (to R. M., H. J. S., and J. M. W.).…”

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Germ Cell Nuclear Factor Relieves cAMP-response Element Modulator τ-mediated Activation of the Testis-specific Promoter of Human Mitochondrial Glycerol-3-phosphate Dehydrogenase

Rajković¹,

Middendorff

Wetzel³

et al. 2004

Journal of Biological Chemistry

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Mitochondrial glycerol-3-phosphate dehydrogenase (mGPDH) is an essential component of the glycerol phosphate shuttle that transfers reduction equivalents from the cytosol into the mitochondrion. Within the testis, immunohistological analysis localized human mG-PDH to late spermatids and to the midpiece of spermatozoa. The expression of human mGPDH is regulated by two somatic promoters, and here, we describe a third testis-specific promoter of human mGPDH. The usage of this testis-specific promoter correlates with the expression of a shortened mGPDH transcript of ϳ2.4 kb in length, which is solely detectable from testicular RNA. Within the testis-specific promoter, we detected a cAMPresponse element (CRE) site at ؊51, which binds the testis-specific transcriptional activator CRE modulator (CREM ) in electrophoretic mobility shift assays. This recognition site overlaps with a nuclear receptor binding half-site at ؊49, which binds the testis-specific transcriptional repressor germ cell nuclear factor (GCNF). Both factors compete for binding to the same DNA response element. Ectopic expression of CREM in HepG2 cells activated a promoter-driven luciferase construct in transient transfection experiments. Additional cotransfection of GCNF relieved this activity, suggesting a down-regulation of CREM -mediated activation by GCNF. This effect was preserved by introducing the CRE/nuclear receptor-binding element into a heterologous promoter context. Our data suggest a down-regulation of CREM -mediated gene expression by GCNF, which might be a general regulation mechanism for several postmeiotically expressed genes with a temporal expression peak during early spermatid development.Mitochondrial glycerol-3-phosphate dehydrogenase (mG-PDH) 1 is an essential component of the glycerol phosphate shuttle. In conjunction with the cytosolic glycerol-3-phosphate dehydrogenase, this shuttle uses the interconversion of glycerol-3-phosphate to dihydroxyacetone phosphate to oxidize cytosolic NADH by transferring reduction equivalents from the cytosol to the mitochondrion (1, 2). The expression of human and rat mGPDH is regulated by two somatic promoters in a tissue-specific manner (3-7), but rat mGPDH is additionally regulated by a third testis-specific promoter (8). The usage of the testis-specific promoter of mGPDH results in a shortened transcript length of ϳ2.4 kb containing an alternate first exon at its 5Ј end and a shortened 3Ј-untranslated region; however, the open reading frame remains unaffected (3,8). In rat testis, mGPDH transcripts have been detected in postmeiotic germ cells during early spermatid development, whereas mGPDH proteins have been detected during late spermatid development (8). The knockout of mGPDH in transgenic mice leads to reduced fertility (9, 10).Within the testis, spermatogenesis is a complex developmental process that includes the mitotic proliferation of spermatogonial stem cells, meiotic prophase, division of spermatocytes, and morphological changes of haploid spermatids to highly specialized spermato...

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Molecular mechanisms of male germ cell differentiation

1998

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cAMP-response element modulator tau is a positive regulator of testis angiotensin converting enzyme transcription.

Cited by 75 publications

References 28 publications

Testis Hormone-sensitive Lipase Expression in Spermatids Is Governed by a Short Promoter in Transgenic Mice

Testis Hormone-sensitive Lipase Expression in Spermatids Is Governed by a Short Promoter in Transgenic Mice

Germ Cell Nuclear Factor Relieves cAMP-response Element Modulator τ-mediated Activation of the Testis-specific Promoter of Human Mitochondrial Glycerol-3-phosphate Dehydrogenase

Molecular mechanisms of male germ cell differentiation

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