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PubMed1986

Promoters of Escherichia coli: a hierarchy of in vivo strength indicates alternate structures.

The strength in vivo of 14 promoters was determined in a system which permits the quantitation of RNA synthesis with high accuracy. Up to 75-fold differences in promoter strength were measured and the most efficient signals are promoters from coliphages T7 and T5. Their activity approaches the strength of fully induced promoters of the rRNA operons which may be close to the functional optimum of a single sequence. By contrast, a synthetic 'consensus promoter' belongs to the less efficient signals. Our data show that optimal promoter function can be achieved by alternate structures and strongly suggest that information outside of the 'classical' promoter region contributes to promoter activity.

Base Sequence↗

PubMed1993

The role of polybasic compounds in determining the tyrosyl phosphorylation of calmodulin by the human insulin receptor.

A highly purified human insulin receptor preparation was shown to effect receptor autophosphorylation and the phosphorylation of poly(GluTyr) but not that of calmodulin. Addition of poly-L-lysine allowed for the stoichiometric tyrosyl phosphorylation of calmodulin in a dose-dependent fashion (EC50 approximately 83 nM) with the single target residue identified at tyr99. Higher concentrations of poly-L-lysine elicited the dose-dependent inhibition of calmodulin phosphorylation (IC50 approximately 0.7 microM) by a process which did not apparently involve either stimulation of calmodulin phosphatase activity or diminished receptor kinase activity. Polybasic substances such as poly-L-arginine, histone H1 and protamine sulphate all promoted calmodulin phosphorylation by the insulin receptor in a similar biphasic dose-dependent fashion. Poly-lysine's actions proved to lack stereo-specificity in that both the D- and L-forms were equally as effective. Reduction in the chain length of poly-L-lysine species attenuated their ability to promote calmodulin phosphorylation with L-lysine proving to be ineffective. Optimal promotion of calmodulin phosphorylation was achieved at an apparently constant ratio of calmodulin to poly-L-lysine of approximately 1:4 over a 100-fold range of calmodulin concentrations. Poly-L-lysine promoted the precipitation and subsequent resolubilization of calmodulin in a fashion whose biphasic dose-dependence paralleled that seen for its action in promoting calmodulin's phosphorylation. NaCl attenuated, in apparently identical dose-dependent fashions, poly-L-lysine's ability to both elicit the precipitation of calmodulin and to promote its phosphorylation. The presence of added Ca2+ led to a small potentiation of poly-L-lysine-dependent calmodulin phosphorylation at low concentrations, with inhibition occurring at higher concentrations where Ca2+ was shown to block calmodulin precipitation by poly-L-lysine. It is suggested that calmodulin can be phosphorylated by the insulin receptor only when it is cross-linked in a multivalent fashion to a suitable polybasic substance so that it forms large multimeric aggregates. Such a requirement for the formation of an aggregate between calmodulin and a suitable polybasic species may place specific constraints on the ability of calmodulin to serve as a substrate for receptor tyrosyl kinases within the cell.

Calmodulin↗

PubMed2003

Nutrition, infection, and periodontal disease.

Even though nutrition is not recognized as a risk factor for periodontal diseases, nutrition is acknowledged to have a significant impact on optimal functioning of the immune response. Dental professionals need to routinely assess nutritional status and provide basic nutrition counseling to their patients to ensure optimal functioning of the immune system in combating infection and to promote optimal periodontal health.

Biofilms↗

PubMed1995

A functional p53-responsive intronic promoter is contained within the human mdm2 gene.

The mdm2 gene is a target for transcriptional activation by the p53 tumor suppressor gene product. Previous work has revealed that the mouse mdm2 gene contains two promoters: one is located upstream to the gene and is active in the absence of p53, the other resides within the first intron and requires p53 for transcriptional activity. To determine whether this unique promoter activation pattern is biologically important, we investigated the structure and function of the corresponding region of the human mdm2 (hmdm2) gene. We report here that the hmdm2 gene also contains an intronic, p53-dependent promoter. The structural features of this promoter are highly conserved between mouse and man, as opposed to the lack of conservation of the first exon. This promoter is triggered in vivo in the presence of activated wild type p53, leading to the production of novel mRNA species. The intronic hmdm2 promoter contains two tandem p53 binding elements. Deletion analysis suggests that optimal promoter activity requires the simultaneous binding of p53 to both elements; this may serve to prevent premature triggering of the promoter by p53.

Animals↗

PubMed2025

Codon Composition in Human Oocytes Reveals Age-Associated Defects in mRNA Decay.

Oocytes from women of advanced reproductive age exhibit diminished developmental potential, but the underlying mechanisms remain incompletely defined. Oocyte maturation depends on translational control of maternal mRNA synthesized during growth. We performed a computational analysis on human oocytes from women <30 versus ≥40 years and observed that mRNA GC content correlates negatively with half-life in oocytes from young (<30 yr) but positively with oocytes from aged (>40 yr) women. In young oocytes, longer mRNA half-life is associated with lower protein abundance, whereas in aged oocytes GC content correlates positively with protein abundance. During the GV-to-MII transition, codon composition stratifies stability: codons that support rapid translation (optimal) stabilize mRNA, while slow-translating codons (non-optimal) promote decay. With reproductive aging, GC-containing codons become more optimal and align with increased protein abundance. These findings indicate that reproductive aging remodels codon-optimality-linked, translation-coupled mRNA decay, stabilizing a subset of GC-rich maternal mRNA that may be prone to excess translation during maturation. Our analysis is explicitly within human reproductive aging; it does not revisit cross-species stability rules. Instead, it shows that sequence-stability relations are reprogrammed with age within human oocytes, including an inversion of the GC-stability association during GV-to-MII transition. Disruption of the normal mRNA clearance program in aged oocytes may compromise oocyte competence and alter maternal mRNA dosage, with downstream consequences for early embryonic development.

Humans↗

PubMed2003

Mechanisms of EDDHA effects on the promotion of floral induction in the long-day plant Lemna minor (L.).

EDDHA added in an optimal concentration (20.5 mumol.L-1) to a modified Pirson-Seidel nutrient solution induces flowering in some clones of the species Lemna minor, Lemna gibba and Spirodela polyrrhiza, which in the absence of EDDHA in the same nutrient solution do not flower. By adding EDDHA (20.5 mumol.L-1), floral induction under LD conditions is optimally promoted in the long-day (LD) species Lemna minor. After adding EDDHA to the nutrient solution, before floral induction and during flowering, Zn, Mn and Cu content is significantly increased in plants. Zn-EDDHA (0.86 mumol.L-1), Mn-EDDHA (1.51 mumol.L-1) and Cu-EDDHA (0.12 mumol.L-1), when used individually, greatly promote flowering under LD conditions as compared to flowering in the same nutrient solution with an equivalent quantity of Zn, Mn or Cu in the nonchelate form. If, on the other hand, Zn-EDDHA and Mn-EDDHA are added to the nutrient solution together (instead of Zn and Mn in nonchelate form), their effect on the promotion of flowering is less than in the case of their individual use. This shows that there is antagonism between Zn-EDDHA and Mn-EDDHA that is eliminated by adding EDDHA to the nutrient solution. We obtained the highest percentage of flowering plants (i.e. 74%) if we added EDDHA (20.5 mumol.L-1) to the nutrient solution containing Mn, Zn and Cu in chelate form. 74% of flowering plants actually means that flowering was achieved in all physiologically mature plants. Our results show that EDDHA promotes floral induction in Lemna minor under LD conditions, especially through chelating Zn, Mn and Cu, and, in addition, through eliminating the antagonism between Mn and Zn chelates EDDHA. Zn-EDDHA (0.86 mumol.L-1) also promote floral differentiation, especially cell division of microspore mother cells into dyads and those into microspore tetrads, which can be seen in microphotographs. When investigating possible pathways through which Mn-EDDHA, Zn-EDDHA and Cu-EDDHA promote flowering, we studied the effects of various concentrations of IAA and sucrose added to the nutrient solution as well. The results support the hypothesis that one of the possible pathways in which Mn-EDDHA promotes floral induction is through auxin oxidase, whereas Zn-EDDHA and Cu-EDDHA probably promote it through the enhancement of the photosynthesis and synthesis of sucrose.

Araceae↗

PubMed2001

Achievement goals and optimal motivation: testing multiple goal models.

Currently, there is a debate about which types of achievement goals promote optimal motivation. A number of theorists argue for a mastery goal perspective focusing on the adaptive consequences of mastery goals and the maladaptive consequences of performance goals. Others endorse a multiple goal perspective in which both mastery and performance goals can be beneficial. The purpose of the present investigation was to review why this debate has emerged and to offer a critical test of the mastery versus multiple goal perspectives. In Study 1, a correlational approach was used to identify the optimal goals for college participants to adopt for a learning activity. In Study 2, an experimental approach was used to identify the optimal goals to assign for the same activity. Each study revealed benefits of both mastery and performance goals, providing support for the multiple goal perspective.

Achievement↗

PubMed1984

Mechanism of CRP-cAMP activation of lac operon transcription initiation activation of the P1 promoter.

CRP-cAMP was shown to activate transcription initiation at the Escherichia coli lac promoter in vitro as a result of two separate effects. An indirect component of the activation resulted from an enhancement of the fraction of promoters productively bound by RNA polymerase. This effect was due largely to CRP-cAMP repression of RNA polymerase binding to an overlapping site (lac P2) within the promoter region. In addition, a direct enhancement of RNA polymerase binding at the principal lac promoter (lac P1) was found. The combination of indirect and direct activation by CRP-cAMP was suggested to be responsible for the large activation observed in vivo. Promoter strength parameters were also determined for the L8, UV5 and Ps promoters. The effect of CRP-cAMP on these mutant promoters was shown to be consistent with the activation mechanism deduced for the lac wild-type promoter. DNA supercoiling enhanced the promoter strength of the lac wild-type and UV5 promoters. The combination of supercoiling and CRP-cAMP was necessary for optimal promoter strength for the lac wild-type promoter.

Cyclic AMP↗

PubMed1997

Regulation of 92 kDa type IV collagenase expression by the jun aminoterminal kinase- and the extracellular signal-regulated kinase-dependent signaling cascades.

The 92 kDa type IV collagenase (MMP-9), which degrades type IV collagen, has been implicated in tissue remodeling. The purpose of the current study was to determine the role of Jun amino-terminal kinase (JNK)- and extracellular signal-regulated kinase- (ERK)-dependent signaling cascades in the regulation of MMP-9 expression. Towards this end, we first determined the transcriptional requirements for MMP-9 promoter activity in a cell line (UM-SCC-1) which is an avid secretor of this collagenase. Transfection of these cells with a CAT reporter driven by progressive 5' deleted fragments of the MMP-9 promoter indicated the requirement of a region spanning -144 to -73 for optimal promoter activity. DNase I footprinting revealed a protected region of the promoter spanning nucleotides -91 to -68 and containing a consensus AP-1 motif at -79. Mutation of this AP-1 motif practically abolished the activity of the MMP-9 promoter-driven CAT reporter. Mobility shift assays indicated c-Fos and Jun-D bound to this motif and transfection of the cells with a mutated c-Jun, which quenches the function of endogenous Jun and Fos proteins, decreased MMP-9 promoter activity by 80%. UM-SCC-1 cells contained a constitutively activated JNK and the expression of a kinase-deficient JNK1 reduced the activity of a CAT reporter driven either by the MMP-9 promoter or by three tandem AP-1 repeats upstream of a thymidine kinase minimal promoter. Conditioned medium collected from UM-SCC-1 cells transfected with the dominant negative JNK1 expression vector diminished 92 kDa gelatinolysis. Similarly, interfering with MEKK, which lies upstream of JNK1, using a dominant negative expression vector reduced MMP-9 promoter activity over the same concentration range which repressed the AP-1-thymidine kinase CAT reporter construct. UM-SCC-1 cells also contained a constitutively activated ERK1. MMP-9 expression, as determined by CAT assays and by zymography, was reduced by the co-expression of a kinase-deficient ERK1. Interfering with MEK1, which is an upstream activator of ERK1, either with PD 098059, which prevents the activation of MEK1, or with a dominant negative expression construct, reduced 92 kDa gelatinolysis and MMP-9 promoter activity respectively. c-Raf-1 is an upstream activator of MEK1 and a kinase-deficient c-Raf-1 expression construct decreased the activity of a promoter driven by either the MMP-9 promoter or three tandem AP-1 repeats. Conversely, treatment of UM-SCC-1 cells with PMA, which activates c-Raf-1, increased 92 kDa gelatinolysis. These data suggest that MMP-9 expression in UM-SCC-1 cells, is regulated by JNK- and ERK-dependent signaling pathways.

Binding Sites↗

PubMed1992

Mapping and characterization of the promoter elements of the regulatory nif genes rpoN, nifA1 and nifA2 in Rhodobacter capsulatus.

The promoter elements responsible for the expression of the regulatory nif genes rpoN, nifA1 and nifA2 of Rhodobacter capsulatus were mapped by exonuclease-III-mediated deletions and by primer extension analysis. The rpoN promoter maps 600 bp upstream of rpoN and has the characteristic features of a -24/-12 promoter. The upstream activator sequence (UAS) displays two mismatches with the NIFA consensus sequence and is located 37 bp upstream of a perfect -24/-12 promoter element. The spacing and/or the helical phasing of these two promotor elements was found to be important for promoter function. In addition, an UAS half-site may contribute to optimal promoter function. The rpoN UAS can partially substitute for the UAS of the nifE promoter. An open reading frame with homology to Klebsiella pneumoniae NIFU was identified between the rpoN promoter and rpoN and termed nifU2 since another nifU-like gene (nifU1) is located in a conventional nifUSVW operon in nif region A. Thus, rpoN, encoding an alternative sigma factor for RNA polymerase, is cotranscribed with a nifU analogous gene from an rpoN-dependent promoter. Mapping of the promoter elements involved in the expression of nifA copy 1 and copy 2 identified a novel promoter type. A conserved distal promoter element is likely to represent the binding site of NTRC in R. capsulatus. The DNA region preceding the mapped 5' ends of the nifA transcripts displays much less homology. The distance between the distal and proximal elements is about 100 bp.

Amino Acid Sequence↗

PubMed1998

ET-1 expression and growth inhibition of prostate cancer cells: a retinoid target with novel specificity.

Endothelin-1 (ET-1) is not only a potent vasoconstrictor but also serves as an important growth stimulator in various cancers, including breast, cervical, pancreatic, and prostate cancer. This suggests that blockage of ET-1 production may suppress tumor growth and possibly metastasis. We observed that certain synthetic retinoids, and all-trans-retinoic acid can repress LNCaP prostate cancer cell growth in vitro. In addition, these retinoid compounds counteracted exogenous ET-1-induced growth stimulation. Retinoid-dependent growth retardation of LNCaP cells coincided with suppression of ET-1 gene expression to a level undetectable by reverse transcription-PCR. Contrarily, the androgen-insensitive DU145 cells were refractory to retinoid treatment. To investigate the underlying mechanisms of the cell-specific response to retinoids, we transfected ET-1 promoter constructs containing wild-type or mutated AP-1 or GATA-2 site into prostate cancer cells. Distinct regulations of ET-1 promoter activity were found; in LNCaP cells, both binding sites are essential for optimal promoter activation, whereas in DU145 cells, additional promoter sequences and/or transcriptional factors seem to be involved. Furthermore, several anti-AP-1 selective retinoids failed to repress ET-1 promoter activity and to exhibit a cell growth-inhibitory effect on LNCaP cells, suggesting that different retinoid structural configurations are required for the inhibition of an AP-1 complex versus an AP-1/GATA-2 complex.

DNA-Binding Proteins↗

PubMed1995

Requirements for optimal expression of secreted and nonsecreted recombinant proteins in vaccinia virus systems.

Selection of an optimal promoter is necessary for efficient expression of foreign genes with vaccinia virus. Since a variety of powerful (homologous) vaccinia virus promoters and foreign (heterologous) promoter systems have been described for use in vaccinia, we have addressed the question of whether a general rule exists that allows the prediction of the optimal promoter/gene combination. We have compared the expression properties of four secreted proteins, the human blood clotting factor IX (FIX), the human blood glycoprotein Protein S (ProtS), the human von Willebrand factor (vWF), and the Hepatitis B virus (HBV) middle surface glycoprotein preS2, with proteins that were reported not to be secreted, the HBV large surface glycoprotein preS1 and the murine leukemia virus (MuLV) BM-5 Eco gag protein. In addition, we have included in our study an internal control protein, the vaccinia virus p11 protein, to monitor possible side effects of the promoter system used. Genes encoding the foreign proteins were placed either under control of a synthetic vaccinia virus early/late promoter (selP) or under control of the bacteriophage T7 promoter (T7/emc system). The secreted proteins were more efficiently expressed when fused to the homologous promoter. Direct comparison of the two promoters indicated that the expression level ranged between 1.4 (ProtS) and 3.9 (FIX)-fold higher with the selP than with the T7 promoter. In contrast, the cell-associated HBV preS1 was more efficiently expressed under the T7 promoter and the MuLV BM-5 Eco gag polypeptide was expressed equally well from both promoters. These data indicate that a careful prediction of optimal promoter/foreign gene combinations for the vaccinia virus expression system is possible. The choice of the optimal promoter/expression system is based on a simple classification scheme, discriminating secreted and nonsecreted proteins.

Animals↗

PubMed2001

The stability of the TFIIA-TBP-DNA complex is dependent on the sequence of the TATAAA element.

To determine the mechanistic differences between canonical and noncanonical TATA elements, we compared the functional activity of two sequences: TATAAA (canonical) and CATAAA (noncanonical). The TATAAA element can support high levels of transcription in vivo, whereas the CATAAA element is severely defective for this function. This dramatic functional difference is not likely to be due to a difference in TBP (TATA-binding protein) binding efficiency because protein-DNA complex studies in vitro indicate little difference between the two DNA sequences in the formation and stability of the TBP-DNA complex. In addition, the binding and stability of the TFIIB-TBP-DNA complex is similar for the two elements. In striking contrast, the TFIIA-TBP-DNA complex is significantly less stable on the CATAAA element when compared with the TATAAA element. A role for TFIIA in distinguishing between TATAAA and CATAAA in vivo was tested by fusing a subunit of TFIIA to TBP. We found that fusion of TFIIA to TBP dramatically increases transcription from CATAAA in yeast cells. Taken together, these results indicate that the stability of the TFIIA-TBP complex depends strongly on the sequence of the core promoter element and that the TFIIA-TBP complex plays an important function in recognizing optimal promoters in vivo.

DNA↗

PubMed1992

Protein binding sites within the human thymidine kinase promoter.

DNase I footprint analysis, using total HeLa cell nuclear extract and purified transcription factor Sp1, was carried out to determine the various protein binding sites within the human thymidine kinase promoter. The promoter has two separate CCAAT elements and multiple Sp1-binding sites, as well as at least one undefined protein binding site. Detailed analysis of protein binding to the two CCAAT elements showed that changing the spacing between the two CCAAT elements altered both protein binding to the distal CCAAT element as well as promoter activity. Both CCAAT elements can act as functional transcription elements, but are not oriented for optimal promoter strength in the human tk promoter. Our studies show that a promoter fragment that has been previously shown to be the minimal region to maintain a serum responsive promoter regulation apparently contains only a single Sp1-binding domain and the more distal of the CCAAT elements.

Base Sequence↗

PubMed2003

Reconstitution of R6K DNA replication in vitro using 22 purified proteins.

We have reconstituted a multiprotein system consisting of 22 purified proteins that catalyzed the initiation of replication specifically at ori gamma of R6K, elongation of the forks, and their termination at specific replication terminators. The initiation was strictly dependent on the plasmid-encoded initiator protein pi and on the host-encoded initiator DnaA. The wild type pi was almost inert, whereas a mutant form containing 3 amino acid substitutions that tended to monomerize the protein was effective in initiating replication. The replication in vitro was primed by DnaG primase, whereas in a crude extract system that had not been fractionated, it was dependent on RNA polymerase. The DNA-bending protein IHF was needed for optimal replication and its substitution by HU, unlike in the oriC system, was less effective in promoting optimal replication. In contrast, wild type pi-mediated replication in vivo requires IHF. Using a template that contained ori gamma flanked by two asymmetrically placed Ter sites in the blocking orientation, replication proceeded in the Cairns type mode and generated the expected types of termination products. A majority of the molecules progressed counterclockwise from the ori, in the same direction that has been observed in vivo. Many features of replication in the reconstituted system appeared to mimic those of in vivo replication. The system developed here is an important milestone in continuing biochemical analysis of this interesting replicon.

Bacterial Proteins↗

PubMed1983

Differential activation of the mouse beta-globin promoter by enhancers.

A series of plasmids was constructed to study the effect of two enhancers, the simian virus 40 72-base-pair repeat and the Harvey sarcoma virus 73-base-pair repeat, on the mouse beta maj-globin promoter. These plasmids contain the mouse beta maj-globin promoter linked to the Escherichia coli galK gene, thus allowing galactokinase enzyme activity to be used as a measure of promoter function. In CV-1 (primate) cells, it was found that an enhancer is required for optimal promoter activity and that the simian virus 40 (primate) enhancer increases galactokinase fourfold more than the Harvey sarcoma virus (mouse) enhancer. In L (mouse) cells, however, the Harvey sarcoma virus enhancer is 1.3-fold stronger than the simian virus 40 enhancer. These data support the hypothesis that enhancer activity can be species specific. Furthermore, when both enhancers are present on the same plasmid, their effect is additive on the beta-globin promoter whether the plasmid is in CV-1 cells or L cells.

Animals↗

PubMed1979

Enhancement of hexose uptake in human polymorphonuclear leukocytes by activated complement component C5a.

The polymorphonuclear leukocyte (PMNL) depends on glucose as a source of energy for motility, chemotaxis, phagocytosis, and bactericidal activity. Activated complement (C5a) at low concentrations stimulates carrier-mediated carbohydrate transport in PMNLs as measured by the uptake of 2-deoxy-D-[(3)H]glucose. Human PMNLs were preincubated at 37 degrees C for 15 min with zymosan-activated human serum or various purified preparations of human C5a. A concentration-dependent increase in deoxyglucose transport (>700% of control) into PMNLs occurred with all test substances. Reaction was linear for 30 min, and uptake of deoxyglucose followed saturation kinetics. C5a caused a decrease in the K(m) for deoxyglucose, from 0.53 to 0.11 mM, without altering the V(max) (44 nmol/30 min per 5 x 10(6) PMNLs in control and 46.6 with C5a). The optimal concentration of C5a for enhanced carrier-mediated transport of deoxyglucose was similar to that which promoted optimal chemotaxis. Activated serum from C5-deficient mice had little or no effect on deoxyglucose transport whereas that from normal syngeneic mice enhanced deoxyglucose transport. C5a did not enhance deoxyglucose transport into isolated erythrocytes, platelets, or lymphocytes. The deoxyglucose within the cell was primarily in the phosphorylated form, and hexokinase activity was not increased in PMNLs stimulated with C5a, indicating that hexokinase was not rate limiting and that enhanced transport was the mechanism of the C5a activity. Insulin at physiologic concentration (10 ng/ml) had no effect on deoxyglucose transport in PMNL and did not act as a competitive inhibitor of C5a. This insulin-like bioactivity could be detected with the amount of C5a that would be present after activation of 0.1-0.5% of the C5 in 1 ml of serum. This suggests that uptake of [(3)H]deoxyglucose by PMNLs might serve as a highly sensitive test for activation of the fifth component of complement.

Biological Transport↗

PubMed2002

Regulation of the gadd45beta promoter by NF-kappaB.

In addition to coordinating immune and inflammatory responses, NF-kappaB/Rel transcription factors control cell survival. The NF-kappaB antiapoptotic function is crucial to oncogenesis, cancer chemoresistance, and to antagonize tumor necrosis factor (TNF) receptor-induced killing. Recently, we have shown that the suppression of the c-Jun-N-terminal kinase (JNK) cascade is a pivotal protective mechanism by NF-kappaB, and that this suppression involves the upregulation of gadd45beta/myd118. Induction of gadd45beta by stress and cytokines requires NF-kappaB; however, the regulatory mechanisms underlying this induction are not known. Here, we report that, in HeLa cells, the NF-kappaB subunit RelA is sufficient to activate gadd45beta expression, whereas Rel and p50 are not. Activation of gadd45beta by RelA depends on three kappaB elements at positions -447/-438 (kappaB-1), -426/-417 (kappaB-2), and -377/-368 (kappaB-3) of the gadd45beta promoter. Each of these sites binds to NF-kappaB complexes in vitro, and is required for optimal promoter transactivation. The data establish the direct participation of NF-kappaB in the regulation of Gadd45beta, thereby providing important mechanistic insights into the control of apoptosis by the transcription factor.

Animals↗