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PubMed2001

Dual enantioselective control in asymmetric synthesis.

It is desirable and practical to produce both enantiomers of a target from the same chiral starting material by stereodifferentiation of prochiral compounds, for instance utilizing a chiral ligand derived from a natural (L) amino acid. During the past 7 years, excellent results have been achieved in several cases by multiple stereodifferentiation of chiral ligands derived from (S)-indoline-2-carboxylic acid: highly diastereo- and enantioselective pinacol coupling reactions of chiral alpha-ketoamides gave both (S,S)- and (R,R)-quaternary tartaric acid for the first time; asymmetric Diels-Alder cyclization of chiral acrylamides in the presence of Lewis acid afforded extremely high diastereoselectivities of both opposite configurations of the cyclized diastereomers depending upon the structures of chiral ligands and Lewis acids; and asymmetric alkylation of aldehydes to both enantiomers of secondary alcohols and asymmetric hydrogenation of ketones to both enantiomers of chiral secondary alcohols have been achieved using catalysts derived from (S)-indoline-2-carboxylic acid.

Journal Article↗
PubMed2005

Dual catalyst control in the enantioselective intramolecular Morita-Baylis-Hillman reaction.

The intramolecular Morita-Baylis-Hillman (MBH) reaction has been achieved with unprecedented levels of enantioselectivity. Using a co-catalyst system involving pipecolinic acid and N-methylimidazole, cyclic MBH products have been obtained with enantiomer ratios of 92:8 (84% ee). In addition, reactions may be carried out with a "kinetic resolution quench" involving acetic anhydride and an asymmetric acylation catalyst such that ee enhancement occurs to deliver products with >98% ee with an isolated yield of 50%. [reaction: see text]

Journal Article↗
PubMed1980

Dual ionic controls for the activation of protein synthesis at fertilization.

The general metabolic activation of the sea urchin egg at fertilization is dependent on a release of intracellular stores of calcium and the subsequent transient elevation of intracellular Ca2+ (refs 1--3). However, this elevation does not by itself lead to increased macromolecular synthesis and development but initiates steps which result in a long-term elevation of intracellular pH (refs 4--6). Among the developmental processes dependent on the elevation of intracellular pH is the large acceleration in the rate of protein synthesis at fertilization. Weak penetrating bases such as ammonia can be used to mimic the processes resulting in an increase in intracellular pH and so show the corresponding increases in protein synthesis rate. Conversely, it is possible to demonstrate a gradual but complete shut down of protein synthesis if the intracellular pH is reduced to the unfertilized level with penetrating weak acids. However, the rate of protein synthesis in ammonia-activated eggs lags behind that of fertilized controls even though ammonia activation can result in an intracellular pH increase greater than occurs in the fertilized egg. This result has led to the suggestion that factors other than intracellular pH may be regulating protein synthesis following fertilization. To investigate the possibility that the Ca2+ transient may have such a role, we measured the rate of amino acid incorporation in eggs that were activated in various ionic conditions which enabled the effects of Ca2+ and pH changes to be studied separately. Our results, reported here, show that if intracellular pH is elevated, increases in intracellular Ca2+ play an additional part in the activation of protein synthesis at fertilization.

Animals↗
PubMed2003

Dual phosphorylation controls Cdc25 phosphatases and mitotic entry.

Negative regulation of the Cdc25C protein phosphatase by phosphorylation on Ser 216, the 14-3-3-binding site, is an important regulatory mechanism used by cells to block mitotic entry under normal conditions and after DNA damage. During mitosis, Cdc25C is not phosphorylated on Ser 216 and ionizing radiation (IR) does not induce either phosphorylation of Ser 216, or binding to 14-3-3. Here, we show that Cdc25C is phosphorylated on Ser 214 during mitosis, which in turn prevents phosphorylation of Ser 216. Mutation of Ser 214 to Ala reconstitutes Ser 216 phosphorylation and 14-3-3 binding during mitosis. Introduction of exogenous Cdc25C(S214A) into HeLa cells depleted of endogenous Cdc25C results in a substantial delay to mitotic entry. This effect was fully reversed in a S214A/S216A double-mutant, implying that the inhibitory effect of S214A mutant was entirely dependent on Ser 216 phosphorylation. A similar regulatory mechanism may also apply to another mitotic phosphatase, Cdc25B, as well as mitotic phosphatases of other species, including Xenopus laevis. We propose that this pathway ensures that Cdc2 remains active once mitosis is initiated and is a key control mechanism for maintaining the proper order of cell-cycle transitions.

14-3-3 Proteins↗
PubMed2006

Dual promoters control the cell-specific expression of the human cell death-inducing DFF45-like effector B gene.

CIDE-B [cell death-inducing DFF45 (DNA fragmentation factor 45)-like effector B] is a member of the CIDE family of apoptosis-inducing factors. The highly restricted pattern of expression of CIDE-B in the liver and spleen suggests that a mechanism exists for the tissue- and cell-specific regulation of transcription of this gene. We have analysed the promoters of the human CIDE-B gene, particularly the mechanism of cell-specific transcription. Expression of CIDE-B is driven by two promoters which are responsible for the synthesis of two types of transcript, and Sp1 and Sp3 are key regulators of basal transcription from both the upstream and the internal promoter, as indicated by EMSAs (electrophoretic mobility-shift assays) and site-directed mutagenesis. Bisulphite sequencing analysis demonstrated that the upstream promoter was hypermethylated in cells that did not express the long transcript of CIDE-B, but was hypomethylated in cells that expressed this transcript. Furthermore, methylation of this region in vitro reduced the promoter activity to approximately 5% of the control. Thus methylation at CpG sites in the upstream promoter region appeared to be important for cell-specific synthesis of the long transcript. By contrast, HNF4alpha (hepatocyte nuclear factor-4alpha) bound to the internal promoter and enhanced its activity. Moreover, the short transcript of CIDE-B gene was expressed in cells which do not normally express this transcript upon introduction of exogenous HNF4alpha, demonstrating the involvement of HNF4alpha in the cell-specific synthesis of the short transcript. Thus our analysis revealed a novel mechanism for the cell-specific transcription of the human CIDE-B gene, which involves epigenetic and genetic control at separate respective promoters.

Apoptosis Regulatory Proteins↗
PubMed2005

Possible role of the 11-cis-retinyl conformation in controlling the dual decay processes of excited rhodopsin.

In this work, we examine how the reported dual decay processes of rhodopsin and binding site stereospecificity can be accounted for by the recently available crystal structure of rhodopsin. Arguments are presented for possible presence of two rhodopsin "rotamers" that fit within the binding cavity. Directed pathways of decay could account for the observed excited decay processes. We summarize evidence for the possible existence of two different ground-state configurations that give rise to two different excited species.

Binding Sites↗
PubMed1983

Carbon starvation and growth rate-dependent regulation of the Escherichia coli ribosomal RNA promoters: differential control of dual promoters.

We studied the effects of carbon starvation and of varying the growth rate on the activity of each of the two tandem ribosomal RNA promoters from the rrnA operon of Escherichia coli. The cellular abundance of plasmid-encoded transcripts arising at promoters P1 and P2 and terminating at the ribosomal RNA terminator in promoter-terminator fusions, together with transcript turnover rates, was used to estimate promoter activities. The rate of synthesis of the P1-promoted transcript was found to increase exponentially with growth rate and predominate at fast growth rates. The activity of the downstream promoter (P2) changed only slightly at different growth rates. Upon carbon starvation, little or no activity of the upstream promoter was detectable, while P2 activity persisted. We interpret this to mean that the dual promoters are differentially regulated so as to have separate adaptive and maintenance functions. This model simplifies most features of rRNA regulation known in E. coli.

Escherichia coli↗
PubMed1995

Dual transcriptional control by Ear3/COUP: negative regulation through the DR1 direct repeat and positive regulation through a sequence downstream of the transcriptional start site of the mouse mammary tumor virus promoter.

Ear3/COUP is an orphan member of the steroid/thyroid hormone receptor superfamily of transcription factors and binds most tightly to a direct repeat of AGGTCA with 1 nucleotide in between (DR1). Ear3/COUP also binds with a similar affinity to the palindromic thyroid hormone response element (TRE). This binding preference of Ear3/COUP is same as that of the retinoid X receptor (RXR), which is another member of the superfamily. In the present study, we identified a sequence responsible for Ear3/COUP-mediated transactivation in the region downstream of the transcription start site of the mouse mammary tumor virus promoter. This cis-acting sequence was unresponsive to RXR. When the DR1 or TRE sequence was added upstream of the promoter, transactivation by Ear3/COUP was completely abolished, whereas RXR enhanced transcription from the promoter. The mode of action of Ear3/COUP could be utilized to control complex gene expressions in morphogenesis, homeostasis, and development.

Animals↗
PubMed1976

Properties of the antigen-specific suppressive T-cell factor in the regulation of antibody response of the mouse. III. Dual gene control of the T-cell-mediated suppression of the antibody response.

The antigen-specific suppressive T-cell factor of mice, which had previously been shown to be an I region gene product, could effectively suppress the in vitro secondary antibody response of spleen cells from syngeneic or H-2 compatible mouse strains but not that of H-2 incompatible strains. The identities among genes in the left side half (K, I-A, and I-B) of the H-2 complex between the donor and recipient strains were found to be both necessary and sufficient for the induction of suppression. This suggests that the acceptor site for the suppressive T-cell factor is also determined by the gene present in the left side half of the H-2 complex. The cell type which expresses the acceptor site was found to be a subset of T cell. In general, the suppressive T-cell factor obtained from F1 mice could suppress the responses of both parental strains, and the parental factors could suppress the response of F1 mice. The results indicate that both suppressor and acceptor molecules are codominantly expressed on F1 T cells. There were found two types of defects in the expression of suppressor and acceptor molecules among mouse strains: A/J mice could not produce the suppressive T-cell factor despite that they could accept the factor produced by other H-2 compatible mouse strains. In contrast, all the B10 congeneic lines could produce the T-cell factor, but could not accept the factor produced by syngeneic and H-2 compatible non-B10 congeneic lines. The F1 hybrid of A/J and B10. A could both produce and accept the T-cell factor, and thus the expressions of suppressor and acceptor molecules were found to be dominant traits. These results indicate that the antigen-specific T-cell-mediated suppression is regulated by at least two genes both present in the H-2 complex, and that the complementation of these two genes is required for the induction of suppression.

Animals↗
PubMed1991

Hybrid PLtl promoter with dual regulation control.

The newly constructed PLtl hybrid promoter is composed of the operator and promoter sequences of tac and the -35 to -135 region of the phage lambda PL promoter, which contains the AT-rich block and the OL2 and OL3 segments. Transcriptional properties of PLtl were examined and compared with tac and lambda PL as reference promoters. The hybrid PLtl exhibits different and improved properties over tac promoter in four ways: (i) when repressed, the repression is almost complete; (ii) after complete induction, the hybrid PLtl promoter shows a 1.4-2 times higher expression; (iii) the hybrid PLtl promoter permits flexible gene expression because it can be utilized under either or both repression controls simultaneously; (iv) the PLtl promoter permits enhanced expression of genes encoding products with unknown properties. When compared with the strong promoter PL from phage lambda, results with the PLtl promoter in lacZ fusion constructs show higher levels of beta-galactosidase activity. We also constructed a plasmid vector, pPLtl7G, which contains the hybrid PLtl promoter with a polylinker sequence at its 3' end, which facilitates efficient fusions of foreign genes in any of the reading frame.

Bacteriophage lambda↗
PubMed2005

Engulfment-regulated proteolysis of SpoIIQ: evidence that dual checkpoints control sigma activity.

During Bacillus subtilis sporulation, the engulfment checkpoint is thought to directly regulate late forespore transcription but to indirectly regulate late mother cell transcription, via the sigmaG-produced protease SpoIVB. We here demonstrate that SpoIIQ is subject to sigmaG-independent, but engulfment-dependent, proteolysis that depends on SpoIVB. Thus, SpoIVB produced before engulfment supports some SpoIVB-dependent events, suggesting that its activity or access to substrates must be regulated by engulfment. Furthermore, a mutation (bofA) that allows sigmaK to be active without sigmaG does not allow sigmaK activity in engulfment mutants, although the pro-sigmaK processing enzyme (SpoIVFB) is localized to the septum in engulfment mutants, suggesting that engulfment comprises a second checkpoint for sigmaK Finally, we find that SpoIIQ and another protein required for sigmaG activity (SpoIIIAH), which directly interact and assemble helical structures around the forespore, recruit the sigmaK-processing enzyme SpoIVFB to the forespore and these structures. We suggest that these foci serve a synapse-like role, allowing engulfment to simultaneously control both sigmaG and sigmaK, and integrating multiple checkpoints and signalling pathways.

Bacillus subtilis↗