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PubMed1992

Role of integration host factor in stimulating transcription from the sigma 54-dependent nifH promoter.

In a wide variety of nitrogen-fixing organisms among the Purple Bacteria (large division of Gram-negative bacteria) the nitrogen fixation (nif) operons are transcribed by an alternative holoenzyme form of RNA polymerase, sigma 54-holoenzyme. Transcription depends on the activator protein NIFA (nitrogen fixation protein A), which catalyzes isomerization of closed complexes between this polymerase and a promoter to transcriptionally productive open complexes. NIFA-mediated activation of transcription from the nifH promoter of Klebsiella pneumoniae is greatly stimulated by the integration host factor IHF, which binds to a site between the upstream binding site for NIFA and the promoter, and bends the DNA. IHF fails to stimulate activation of transcription from this promoter by another activator of sigma 54-holoenzyme, NTRC (nitrogen regulatory protein C), which lacks a specific binding site in the nifH promoter region. As predicted, if the IHF-induced bend facilitates interaction between NIFA and sigma 54-holoenzyme, substitution of an NTRC-binding site for the NIFA-binding site allowed IHF to stimulate NTRC-mediated activation of transcription from the nifH promoter. The stimulation was of the same order of magnitude as that for NIFA in the native configuration of the promoter-regulatory region (up to 20-fold). With purified NTRC and the substitution construct we could demonstrate that stimulation by IHF in a purified transcription system was comparable to that in a crude coupled transcription-translation system, indicating that the stimulation in the crude system could be accounted for by IHF. The IHF stimulation was observed on linear as well as supercoiled templates, indicating that the geometric requirements are relatively simple. We have attempted to visualize the arrangement of proteins on DNA fragments carrying the nifH promoter-regulatory region of K. pneumoniae by electron microscopy. IHF stimulated NIFA-mediated activation of transcription from the nifH and nifD promoters of Bradyrhizobium japonicum and less so from the nifH promoters of Rhizobium meliloti and Thiobacillus ferrooxidans, consistent with previous observations that stimulation is greatest at promoters that are weak binding sites for sigma 54-holoenzyme in closed complexes.

Bacterial Proteins↗
PubMed1992

DNA supercoiling response of the sigma 54-dependent Klebsiella pneumoniae nifL promoter in vitro.

Transcription from the sigma 54-dependent Klebsiella pneumoniae nifL and glnAp2 promoters is activated by the general nitrogen regulatory protein NTRC. Unlike the glnAp2 promoter, which is relatively insensitive to changes in DNA supercoiling, transcription from nifL in vitro in a chloride-based buffer is supercoiling-dependent at physiological salt concentrations. The replacement of chloride with an acetate-based buffer decreases the stringency of the nifL supercoiling response, but open complexes formed on linear nifL promoter DNA under these conditions are unstable and less extensive than those found on supercoiled (form I) DNA. We have introduced mutations in particular elements of the nifL promoter that increase its homology to glnAp2. At the wild-type nifL promoter, sigma 54-RNA polymerase makes only limited contacts with the promoter in the absence of NTRC. However, a G to T change at -26 (nifL74) allows the formation of a stable closed complex with sigma 54-holoenzyme on both linear and form I templates in the absence of the activator. The combination of C to T mutations at -3 and -1 (nifL18) increases the A+T rich nature of the melted region and stabilizes open complexes formed on linear DNA. Open complex formation as a function of superhelical density was assessed at each promoter. Formation of open complexes at glnAp2 peaks at -0.024 and declines at higher superhelical densities, whereas at the wild-type nifL promoter, open complex formation peaks at -0.067 and is not detectable at superhelical densities less than -0.032. Both the nifL74 and nifL18 mutations altered the supercoiling response, increasing the ability to form open complexes at low superhelical densities. The presence of the nifL74 and nifL18 mutations in combination further altered the response of the promoter to DNA supercoiling. These observations suggest that the promoter as a whole, and not any one promoter element, mediates the transcriptional response to DNA supercoiling.

Base Sequence↗
PubMed1992

DNA topology-mediated regulation of transcription initiation from the tandem promoters of the ilvGMEDA operon of Escherichia coli.

It is becoming increasingly clear that the intrinsic and protein-induced topological properties of the DNA helix influence transcriptional efficiency. In this report we describe the properties of two upstream activating regions that influence transcription from the non-overlapping tandem promoters of the ilvGMEDA operon of Escherichia coli. One 20 base-pair region between the promoter sites contains an intrinsic DNA bend that activates transcription from the downstream promoter. The other region contains an integration host factor (IHF) binding site that overlaps the upstream promoter site. IHF binding at this site represses transcription from the upstream promoter and enhances transcription from the downstream promoter. IHF also induces a severe bend in the DNA at its target binding site in the upstream promoter region. The activating property of the 20 base-pair DNA sequence located between the promoters is dependent upon the helical phasing of the sequence-directed DNA bend that it encodes. However, the IHF-mediated activation of transcription is not dependent upon the helical phasing (spatial orientation) of the upstream IHF and downstream promoter sites. The IHF-mediated activation of transcription is also uninfluenced by the presence or absence of the intrinsic DNA bend between its binding site and the downstream promoter site. These results suggest the interesting possibility that IHF activates transcription from the nearby downstream promoter simply by bending the DNA helix in the absence of specific IHF-RNA polymerase or upstream DNA-RNA polymerase interactions.

Bacterial Proteins↗
PubMed1988

Functional anatomy of the simian virus 40 late promoter.

We have examined the control sequences for the late promoter function of simian virus 40 (SV40) in COS-1 cells which produce SV40 T antigen constitutively. Plasmids were constructed by cloning mutant late promoter segments upstream from sequences coding for the bacterial chloramphenicol acetyltransferase (CAT) gene, and were converted to "double-origin" type by inserting functional replication origin segments downstream from the CAT gene for replicative competence when necessary. The late promoter activity was determined by transient expression assay of the CAT mRNA and enzyme activity levels following DNA-mediated gene transfer into COS-1 cells. We find that the minimal replication origin and the 21-bp repeat containing T antigen and transcription factor Sp1 binding sites, respectively, are dispensable for late promoter function provided that one copy of the 72-bp repeat enhancer is present. We have mapped within the 72-bp repeat the major late promoter component in a 68-bp fragment (located between nucleotides 205 and 272), and found an overlapping 55-bp fragment (located between nucleotides 179 and 234) to have about one-fifth of the late promoter activity. Both the 68- and 55-bp fragments lack some of the core sequence elements required of the 72-bp repeat for transcriptional enhancer activity, and lack the ability to enhance the activity of the SV40 early promoter. The results suggest that the organization of functional units of the 72-bp repeat required for transcriptional enhancement of the early promoter is different from that required for late promoter function. The 21-bp repeat was found to have some late promoter activity located within the origin-distal copy in the absence of the 72-bp repeat. In association with the 21-bp repeat, the otherwise dispensable origin-proximal 22-bp of the 72-bp repeat containing activator protein AP-1 binding site augmented late promoter activity by three- to fourfold.

Antigens, Viral, Tumor↗
PubMed1996

Identification and characterization of two promoters of rat kallikrein-binding protein gene.

Rat kallikrein-binding protein (RKBP) is a serine proteinase inhibitor (serpin) which binds to and inhibits tissue kallikrein activity [1,2]. In this study, we have sequenced and identified two promoter regions of the RKBP gene (RKBP). One promoter is located in the 5' flanking region (P1) of the gene and the other is located in the first intron (P2). Both promoters contain a consensus TATA and CAAT box. These RKBP promoters were fused with a chloramphenicol acetyltransferase (CAT) reporter gene and their promoter activities were determined by measuring CAT levels using a specific ELISA. The P1 promoter exhibited high promoter activities in Hep3B hepatoma cells but not in La-fibroblastoma cells, indicating its tissue-specificity. By deletion analysis, we have identified a negative regulatory element of the P1 promoter between -739 and -472, and defined a minimal sequence between -183 and -2 for maintaining the intact promoter activity. The P2 promoter showed a strong activity only when linked to an SV40 enhancer. Activity of the P1 promoter can be induced by growth hormone in Hep3B cells. Gel retardation assay has identified 5 DNA fragments which were bound by nuclear proteins from rat liver. Two DNA fragments are in the 5' flanking region, one contains a putative glucocorticoid and growth hormone response element and the other one contains a CAAT box and two putative AP-1 binding sites. The remaining three are in the first intron and contain a putative thyroid hormone response element, a putative GATA site and three consensus CAAT boxes, respectively. Nuclear proteins from the kidney showed that spontaneously hypertensive rats (SHR) have a distinct trans-acting factor which binds with the DNA fragment containing the glucocorticoid and growth hormone response elements, as compared with normotensive rats. This result indicates that different trans-acting factors in the kidney of SHR may contribute to the decreased RKBP expression in these hypertensive rats.

Animals↗
PubMed1984

Mutants of the lac promoter with large insertions and deletions between the CAP binding site and the -35 region.

A set of the lac promoter mutants that have varying lengths of the spacer between the CAP binding site and the -35 region was constructed. The mutants have the spacer length increased by five (I5 mutant), or eleven (I11) residues or decreased by eleven residues (D11). We also present a construction of the hybrid between the gal and lac promoters in which the CAP binding site and the -35 region of the gal promoter are fused to the lac -10 region. The promoter fragments were assembled through ligations of chemically synthesized oligodeoxynucleotides and cloned into a pBR322-derivative vector. The results of the in vivo assays of promoter activity show that the I11 mutation results in an active but weak promoter that can be stimulated by CAP, though to a lesser degree than the wild-type lac promoter. The other mutants exhibit no promoter activity. Since the insertion of 11-bp preserves the location of the CAP binding site on the same side on the DNA helix, the data demonstrate the importance of spatial alignment between the CAP binding site and the promoter. The fact that the gal::lac hybrid is inactive as a promoter indicates also that catabolite activation is a highly complex process in which the -35 and -10 regions cannot be easily exchanged between promoters.

Base Sequence↗
PubMed1986

Analysis of promoter and enhancer cell type specificities and the regulation of immunoglobulin gene expression.

We have analysed the properties of IgH promoter (VH) and enhancer (Ig) regions which were used to drive the expression of the chloramphenicol acetyl transferase (CAT) gene (cat) in recombinant plasmids. We observe little synergistic effect between the VH promoter and Ig enhancer on cat gene expression in our constructs. Replacing the VH promoter by the thymidine kinase (TK) promoter does not affect the enhancer-mediated B-cell-specific expression of the cat gene. However, replacement of the VH promoter by the mouse renin gene promoter, which is not normally expressed in B cells, completely abolishes cat gene expression in cells of this lineage. When the Ig enhancer is replaced by the SV40 enhancer (SV), CAT activity is restricted to B cells. The VH promoter is as efficient as the TK promoter in a preB cell line. Extending the size of the VH promoter fragment to include sequences between 126 to 639 bp upstream from the transcription start point results in an eight-fold decrease in CAT activity. In this situation, the tissue specificity of the promoter cat fusion is maintained. Among the various combinations tested here, the association of the TK promoter and the Ig enhancer expresses the cat gene most efficiently. The implications of these observations are discussed.

Acetyltransferases↗
PubMed1987

Two promoters from the Streptomyces plasmid pIJ101 and their expression in Escherichia coli.

An RNA polymerase-binding restriction fragment from the small, high-copy-number Streptomyces plasmid pIJ101 has been shown to have promoter activity in vivo using a promoter-probe vector. The nucleotide sequence of the promoter (the pIJ101B promoter) and the approximate position of the transcription start point as identified by in vitro run-off transcription are presented. Both the pIJ101B promoter and the previously characterised pIJ101A promoter were found to promote transcription in Escherichia coli. The transcription start point in E. coli for the pIJ101A promoter has been determined using high-resolution S1 mapping. Initiation occurs at the same point or within 1 or 2 nucleotides of the transcription start point previously identified in Streptomyces lividans, indicating that the same transcriptional signals are recognised in both genera. The data support the idea that one type of RNA polymerase holoenzyme in Streptomyces recognises a class of promoters similar to the major consensus promoters of E. coli, and that the manner of promoter recognition is similar in both genera.

Base Sequence↗
PubMed2005

Regulatory studies of murine methylenetetrahydrofolate reductase reveal two major promoters and NF-kappaB sensitivity.

Two promoters of the murine methylenetetrahydrofolate reductase gene (Mthfr), a key enzyme in folate metabolism, were characterized in Neuro-2a, NIH/3T3 and RAW 264.7 cells. Sequences of 189 bp and 273 bp were sufficient to achieve maximal activity of the upstream and downstream promoter, respectively. However, subtle differences in minimal promoter lengths and in promoter activities were observed between the cell lines. Both promoters demonstrated comparable activity in NIH/3T3 and RAW 264.7 cells, while in Neuro-2a cells, the upstream promoter was 15-fold more active than the downstream promoter. Alignment and data mining tools identified a candidate nuclear factor kappa B (NF-kappaB) binding site at the 3'end of the downstream promoter that is conserved throughout several species. NF-kappaB activation experiments in cultured cells were associated with increased Mthfr mRNA. Co-transfection of NF-kappaB and promoter constructs demonstrated Mthfr up-regulation by at least 2-fold through its downstream promoter in Neuro-2a cells; this increase was significantly reduced when the putative binding site was mutated. EMSA analysis demonstrated direct binding of NF-kappaB to this non-mutated site. This study, a first step into the elucidation of Mthfr regulation, demonstrates that two TATA-less, GC-rich promoters differentially drive transcription of Mthfr in a cell-specific manner, and provides a novel link of Mthfr to possible roles in the immune response and cell survival.

3T3 Cells↗
PubMed2006

Assay and characterization of a strong promoter element from B. subtilis.

A new strong promoter fragment isolated from Bacillus subtilis was identified and characterized. Using the heat stable beta-galactosidase as reporter, the promoter fragment exhibited high expression strength both in Escherichia coli and B. subtilis. The typical prokaryotic promoter conservation regions were found in the promoter fragment and the putative promoter was identified as the control element of yxiE gene via sequencing assay and predication of promoter. To further verify and characterize the cloned strong promoter, the putative promoter was sub-cloned and the beta-Gal directed by the promoters was high-level expressed both in E. coli and B. subtilis. By means of the isolated promoter, an efficient expression system was developed in B. subtilis and the benefit and usefulness was demonstrated through expression of three heterologous and homogenous proteins. Thus, we identified a newly strong promoter of B. subtilis and provided a robust expression system for genetic engineering of B. subtilis.

Bacillus subtilis↗
PubMed2005

DNA immunization using a non-viral promoter.

Most DNA vaccines rely on strong viral promoters to optimize levels of transgene expression. Some studies have demonstrated that the potency of viral promoters does not necessarily correlate with DNA vaccine efficacy in vivo. This has partly been attributed to downregulation of these promoters by cytokines such as interferon gamma induced by the CpG motives of these vaccines. In an attempt to avoid downregulation of viral promoters by IFN-gamma, we tested vaccine vectors driven by the MHC class II promoter. To enhance the activity of this promoter, another plasmid expressing the human MHC class II transactivator driven by a viral promoter, the native IFN-gamma inducible CIITA type IV promoter (PIV) or a synthetic promoter containing IFN-gamma inducible elements was co-inoculated. Our data show that a non-viral promoter such as the MHC class II promoter tested in this study can indeed be used in DNA vaccines.

Animals↗
PubMed2004

Transcriptional targeting in ovarian cancer cells using the human epididymis protein 4 promoter.

OBJECTIVE: Limitations of current ovarian cancer gene therapies include lack of specificity and transduction of normal tissues. One strategy toward overcoming these limitations is to direct gene therapy specifically to ovarian cancer cells by using tissue- and tumor-specific promoters. The whey-acidic protein human epididymis protein 4 (HE4) is frequently overexpressed in ovarian cancer, suggesting that the HE4 promoter is highly transcriptionally active in the disease. The objective of this study was to isolate the HE4 promoter and examine its ability to selectively activate reporter gene expression in an ovarian cancer-specific manner. METHODS: To investigate transcriptional targeting in ovarian cancer gene therapy, we isolated a region of the HE4 promoter from -530 to +122 (pHE4-652; relative to the ATG start site of HE4) and placed it upstream of a luciferase reporter gene plasmid to generate pHE4-652-luc. The activity of the pHE4-652-luc reporter construct was characterized in transient transfection assays in a panel of epithelial ovarian cancer cell lines (SKOV-3, SKOV-3x, CP70, HeyC2, A2780, A2780CP, OVCAR-3), non-ovarian tumor cell lines, and primary cultures of normal cells. The activity of two other candidate gene therapy promoters, human telomerase reverse transcriptase (hTERT) and OSP1, was also characterized in these cell lines. RESULTS: The HE4 promoter was active in 5/7 ovarian cancer cell lines with the range of activity spanning 0.06- to 3-fold that observed for a positive control, cotransfected reporter construct (SV-40-luc). Minimal pHE4-652 promoter activity, defined as < or =5% of the activity detected with the SV-40-luc construct, was observed in the non-ovarian tumor cell lines and normal cells. The hTERT and the OSP1 promoters were active in the ovarian cancer lines. hTERT activity was highest in the CP70 cell line, and OSP1 activity was highest in the SKOV-3x cell line. Modest OSP1 and hTERT promoter activity was observed in normal cell lines and in selected non-ovarian cancer cell lines. CONCLUSION: This is the first report using the pHE4-652 promoter to drive specific reporter gene expression in epithelial ovarian cancer cell lines, and we are continuing to develop this promoter for use in transcriptional targeting in ovarian cancer gene therapy.

Cell Line, Tumor↗
PubMed2002

The human DNA methyltransferases DNMT3A and DNMT3B have two types of promoters with different CpG contents.

DNA modification that is established by de novo methylation is involved in the epigenetic control of genome functions. The DNMT3A and DNMT3B genes encode putative de novo methyltransferases. In this paper, we investigated the transcriptional regulatory regions of the human DNMT3A and DNMT3B genes. We found that the DNMT3A and DNMT3B genes have multiple transcriptional start points (TSPs) that are separated on the chromosome and the expressions of these genes are controlled by multiple promoters. The DNMT3A gene has at least four TSPs and the expression is controlled by three different promoters. All three promoters lack typical TATA sequences adjacent to the TSPs. Two of them bear CpG-rich promoters and the other a CpG-poor promoter. The DNMT3B gene has at least two TSPs which exist in different exons and the expression is controlled by different promoters. Both promoter regions of the DNMT3B gene lack typical TATA sequences, where one promoter contains a CpG-rich area near the TSP, the other promoter is CpG-poor. Together with the data that the human DNMT1 gene has both CpG-rich and CpG-poor promoters, it is suggested that transcriptional regulation by two types of promoters, CpG-rich and CpG-poor, might be common characteristics in the DNMT gene family.

5' Flanking Region↗
PubMed1998

Structural analysis of the human RFC-1 gene encoding a folate transporter reveals multiple promoters and alternatively spliced transcripts with 5' end heterogeneity.

The organization and structure of the human RFC-1 gene encoding a folate transporter were determined. The RFC-1 gene spans 22.5kb and was found to be distributed in eight exons, including five primary exons and three alternatives of exon 1. Most splice junctions conform to consensus sequences for such junctions. The human RFC-1 gene differs from the mouse and hamster genes both in terms of the total number of exons and in regard to alternatives of exon 1 which encode 5' end heterogeneity. Previously described cDNA variants (GenBank/EMBL accession no. U19720) are now shown to incorporate one of two alternatives (exons 1a and 1b) to exon 1 and exons 2-6 as a result of RNA splicing. Another variant also described may not be full length in that it incorporates a probable alternative (exon 1c) to exon 1 along with exon 2 and a truncated exon 3. A relatively GC- rich region of the genome 5' of the alternatives to exon 1 appears to be distinctly promoter like and incorporates a number of putative cis-acting elements, including multiple SP1 sites, involved in the regulation of transcription. Primer extension analysis of this upstream region in two human cell types revealed a similar pattern of multiple transcription start sites (tsp) proximal to the 5' end of exon 1. However, there was a greater number of potential tsp within the region immediately upstream of exon 1b than within the regions upstream of exons 1a and 1c. The existence of true alternatives to exon 1 in this gene incorporating different 5' ends indicates that its transcription is under the control of multiple promoters. The identity of two such promoters was obtained by functional deletion analysis, showing that expression of a luciferase reporter gene was directed separately by discrete stretches of nucleotide sequence proximal to exon 1a (promoter 1) or exon 1b (promoter 2) in transient transfection experiments. Promoter 1 appeared to have a three-fold lower basal activity than promoter 2, but was enhanced up to nine-fold in fusion constructs containing an SV40 enhancer element. Also, promoter 2 partly consists of a highly GC-rich direct repeat element containing at least three putative SP-1 and 3 putative MZF1 sites. Finally, the activity of these promoters relative to each other was consistent with the results of primer extension analysis showing a greater multiple and usage of tsp within promoter 2 (exon 1b) than within promoter 1 (exons 1a and 1c), suggesting that the variant incorporating exon 1b was the most abundant.

Alternative Splicing↗
PubMed1999

Transcription of the mouse RFC-1 gene encoding a folate transporter. Multiplicity and properties of promoters with minimum requirements for their basal activity.

The mouse RFC-1 gene incorporates alternates of exon 1 (exon 1 and 1a) which encode different 5' ends. This finding, and the elucidation of a promoter-like sequence immediately upstream of these alternates of exon 1, suggest that two separate promoters drive transcription of this gene. The regions upstream of either exon 1 or exon 1a inserted in pGL3 will separately promote transcription in NIH3T3 cells of the luciferase reporter gene, with the region upstream of exon 1 having the strongest promoter activity. Tissue-specific expression in the form of RFC-1 mRNA splice variants reflects the separate action of each promoter. In the most upstream portion of the region proximal to exon 1a, elements were revealed that enhance transcription along with a more downstream element that suppresses transcription in NIH3T3 cells. Three Sp1 sites closely proximal to exon 1a within a region spanning 123 nucleotides were shown to be transcriptionally active by site-directed mutagenesis, with the middle SP1 site found to be the most important of the three in maintaining basal promoter activity. A poly (GT) 21 di-nucleotide repetitive element upstream of these Sp1 sites was found in a region which, when deleted, increased transcription. In the region upstream of exon 1, two elements were elucidated which enhanced transcription. Site-directed mutagenesis showed that two adjacent SP1 sites proximal to exon 1 were equally important in sustaining basal promoter activity. The role of each Sp1 site in maintaining basal activity of each promoter was confirmed by DNase I footprinting analysis. In addition, a binding site of unknown significance was identified by this analysis within the upstream promoter sequence between the two Sp1 sites proximal to exon 1a. These data show that both promoters regulating expression of the RFC-1 gene utilize closely spaced Sp1 sites in tandem to sustain basal transcription, at least in NIH3T3 cells, in a manner characteristic of TATA-less promoters.

3T3 Cells↗
PubMed2002

Selective recruitment of TAFs by yeast upstream activating sequences. Implications for eukaryotic promoter structure.

The general transcription factor TFIID is composed of the TATA box binding protein (TBP) and multiple TBP-associated factors (TAFs). In yeast, promoters can be grouped into two classes based on the involvement of TAFs. TAF-dependent (TAF(dep)) promoters require TAFs for transcription, and TBP and TAFs are present at comparable levels on these promoters. TAF-independent (TAF(ind)) promoters do not require TAFs for activity, and TAFs are either absent or present at levels far below those of TBP on these promoters. Here, we demonstrate that the upstream activating sequence (UAS) mediates the selective recruitment of TAFs to TAF(dep) promoters. A TAF(ind) UAS fails to recruit TAFs and to direct efficient transcription when inserted upstream of a TAF(dep) core promoter. This transcriptional defect can be overcome by a potent activator, indicating that a strong activation domain can compensate for the absence of TAFs on a TAF(dep) core promoter. Our results reveal a requirement for compatibility between the UAS and core promoter and thus help explain previous reports that only certain yeast UAS-core promoter combinations and mammalian enhancer-promoter combinations are efficiently transcribed. The differential recruitment of TAFs by UASs provides strong evidence for the proposal that in vivo TAFs are the targets of some, but not all, activators.

Promoter Regions, Genetic↗
PubMed2001

Acculturation and interrelationships between problem and health-promoting behaviors among Latino adolescents.

PURPOSE: To examine: (a) the effects of acculturation on a healthy lifestyle including problem behaviors (substance use and sex acts) and health-promoting behaviors (e.g., seat belt use, vitamin intake, hours of sleep per night) and (b) the interrelationships among problem and health-promoting behaviors among Latino adolescents. METHODS: Face-to-face interviews were conducted with Latino adolescents (n = 609) with questions covering the following areas: acculturation, sociodemographics, problem behaviors, and health-promoting behaviors. The participants ranged in age from 11 to 19 (mean = 15) years. Bivariate correlations and factor analyses were used to examine the relationship between problem and health-promoting behaviors. A combination of one-way analyses of variance (ANOVAs), Chi-square tests, and Student's t-tests were used to analyze the effects of acculturation on problem and health-promoting behaviors. RESULTS: Higher levels of acculturation were associated with an increased likelihood of exhibiting problem behaviors and a decreased likelihood of exhibiting certain health-promoting behaviors. Foreign-born Latinos were significantly less likely to engage in problem behaviors. Problem behaviors were likely to co-occur; however, the co-occurrence of health-promoting behaviors was not evident. The results also revealed the co-occurrence of problem behaviors with selected health-promoting behaviors. CONCLUSIONS: Among Latino adolescents, there seems to be evidence that problem behaviors and certain health-promoting behaviors do co-occur. To the extent that "healthy lifestyles" are conceptualized as the presence of health-promoting behaviors and the absence of problem behaviors, less acculturated Latino adolescents seem to fare better than those that are more acculturated. Interventions to promote "healthy lifestyles" among Latino adolescents should be tailored to take into consideration the effect of acculturation.

Acculturation↗
PubMed1995

Human sterol carrier protein x/sterol carrier protein 2 gene has two promoters.

The human sterol carrier protein x (SCPx)/sterol carrier protein 2 (SCP2) gene gives rise to two mRNAs: a 2.8 kb mRNA encoding SCPx, a peroxisome-associated thiolase, and a 1.5 kb mRNA encoding SCP2, which is thought to be an intracellular lipid transfer protein. The SCPx/SCP2 gene is highly expressed in organs involved in lipid metabolism, but the relative abundance of SCPx and SCP2 mRNAs varies. Here we report that the two transcripts are produced under the direction of two independent promoters. We determined the DNA sequence of 3.4 kb of the proximal promoter governing the transcription of SCPx sequences. The promoter governing the transcription of SCP2 sequences was identified 45 kb downstream from the SCPx promoter in intron XI. This promoter initiates transcription within exon XII. Both the SCPx and SCP2 promoters lack TATA boxes and initiate transcription at multiple sites. They share features that are found in the promoters of genes encoding other peroxisomal proteins. The basal activities of the two promoters were tested as fusion gene constructs in selected host cells, including BeWo choriocarcinoma cells, HepG2 hepatoblastoma cells, murine Y1 adrenocortical tumor cells, and Balb 3T3 fibroblasts. Cell host-specific patterns of promoter activity were observed. In addition, 8-Br-cAMP and phorbol myristate acetate were found to increase SCPx promoter activity in a host cell-specific manner. The SCP2 promoter was not significantly influenced by these agents.(ABSTRACT TRUNCATED AT 250 WORDS)

3T3 Cells↗