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PubMed1986

Regulation of Cytokinin Oxidase Activity in Callus Tissues of Phaseolus vulgaris L. cv Great Northern.

The regulation of cytokinin oxidase activity in callus tissues of Phaseolus vulgaris L. cv Great Northern has been examined using an assay based on the oxidation of N(6)-(Delta(2)-isopentenyl)adenine-8-(14)C (i(6) Ade-8-(14)C) to adenine. Solutions of exogenous cytokinins applied directly to the surface of the callus tissues induced relatively rapid increases in cytokinin oxidase activity. The increase in activity was detectable after 1 hour and continued for about 8 hours, reaching values two- to three-fold higher than the controls. The cytokinin-induced increase in cytokinin oxidase activity was inhibited in tissues pretreated with cordycepin or cycloheximide, suggesting that RNA and protein synthesis may be required for the response. Rifampicin and chloramphenicol, at concentrations that inhibited the growth of Great Northern callus tissues, were ineffective in inhibiting the increase in activity. All cytokinin-active compounds tested, including both substrates and nonsubstrates of cytokinin oxidase, were effective in inducing elevated levels of the enzyme in Great Northern callus tissue. The cytokinin-active urea derivative, Thidiazuron, was as effective as any adenine derivative in inducing this response. The addition of Thidiazuron to the reaction volumes used to assay cytokinin oxidase activity resulted in a marked inhibition of the degradation of the labeled i(6) Ade-8-(14)C substrate. On the basis of this result, it is possible that Thidiazuron may serve as a substrate for cytokinin oxidase, but other mechanisms of inhibition have not yet been excluded.

Journal Article↗

PubMed2004

Medication reviews in the community: results of a randomized, controlled effectiveness trial.

AIMS: To examine the effectiveness of a multidisciplinary service model delivering medication review to patients at risk of medication misadventure in the community. METHODS: The study was carried out in three Australian states; Queensland, New South Wales and Western Australia, and conducted as a randomized, controlled effectiveness trial with the general practitioner (GP) as the unit of randomization. In total, 92 GPs, 53 pharmacists and 400 patients enrolled in the study. The multidisciplinary service model consisted of GP education, patient home visits, pharmacist medication reviews, primary healthcare team conferences, GP implementation of action plans in consultation with patients, and follow-up surgery visits for monitoring. Effectiveness was assessed using the four clinical value compass domains of (i) functional status, (ii) clinical outcomes, (iii) satisfaction and (iv) costs. The domains of functional status (assessed by the health-related quality of life measure SF-36 subscales) and clinical outcomes (as assessed by adverse drug events (ADEs), number of GP visits, hospital services and severity of illness) were measured at baseline and endpoint. Satisfaction was measured by success in implementation and by participant satisfaction at endpoint, and costs (as assessed using medication and healthcare service costs, less intervention costs) were measured preintervention and during the trial. In addition, process evaluation was conducted for intervention patients, in which problems and recommendations from the medication reviews were described. RESULTS: The model was successfully implemented with 92% of intervention GPs suggesting that the model had improved the care of participating patients, a view shared by 94% of pharmacists. In addition, positive trends in clinical outcomes (ADEs and severity of illness) and costs (an ongoing trend towards reduction in healthcare service costs) were evident, although the trial was limited to a 6-month intervention time. No differences between intervention and control groups were identified for the health-related quality of life domain. The cost-effectiveness ratio for the intervention based on cost savings, reduced adverse events and improved health outcomes was small. The most common problems identified in the medication reviews were potential adverse drug reactions, suboptimal monitoring and adherence/lack of concordance issues. In total, 54.4% of recommendations were enacted, and 23.9% were implemented precisely as recommended in the medication review. Follow-up evaluation showed that 70.9% of actions had a positive outcome, 15.7% no effect and 3.7% had a negative outcome. CONCLUSIONS: Most studies emphasize efficacy and the best achievable clinical outcomes rather than whether an intervention will be effective in practice. The current trial showed that three of the four domains in the clinical value compass showed trends of improvement or were indeed improved in the relatively short follow-up period of the trial, suggesting that a service based on this model could achieve similar benefits in practice. A domiciliary medication review programme similar to this model has now been implemented into national Australian practice, where GPs and pharmacists are reimbursed by the Australian government for the provision of these services.

Adult↗

PubMed2006

Towards profiling the gene expression of fibroblasts from atopic dermatitis patients: human 8K complementary DNA microarray.

BACKGROUND: High-throughput technologies, including DNA-chip array, have been used to search for the genes that are dysregulated in human diseases. The atopic dermatitis (AD)-associated genes are gradually being reported; however, the differentially altered gene expression profiles of atopic fibroblasts have not been well elucidated. OBJECTIVE: We wanted to gain more insights into AD and to find candidate genes, especially in regards to the role of fibroblasts in the pathogenesis of AD. METHODS: cDNA microarray (8K) profiling of the primary cultured AD patients-derived fibroblasts was conducted by a pooling method of the recruited 22 normal controls, the 10 extrinsic type (ADe) patients and the 10 intrinsic type (ADi) patients. SAM analysis of the microarray results (2-fold cut-off) was conducted to select the candidate genes. Quantification by real-time PCRs confirmed the array data in the randomized paired samples (normal vs. ADe n=10; normal vs. ADi n=10). RESULTS: We listed the 22 up-regulated and 95 down-regulated genes in the AD fibroblasts. Real-time PCR results showed that several genes such as hyaluronan synthase 2 (HAS2), TNF-alpha-induced protein 6 (TNFAIP6) and IL-8 were matched with the array results with statistical significance. CONCLUSION: These results suggest gene expression profiles that are associated with AD and this implied that fibroblasts may play important roles in the AD pathogenesis. We provided new insights into three candidate genes such as HAS2, TNFAIP6 and IL-8 with respect to their involvement in AD disease.

Adult↗

PubMed2005

Transcriptional regulation of the one-carbon metabolism regulon in Saccharomyces cerevisiae by Bas1p.

The mechanisms mediating responses to glycine withdrawal in budding yeast were studied using a genome-wide profiling approach. A striking pattern of repressed expression of genes with an enrichment for those involved in one-carbon metabolism and AMP biosynthesis was revealed. Sequence analysis of the promoters for the most severely repressed genes identified a conserved sequence, TGACTC, a known binding site for the transcription factors Gcn4p and Bas1p. Loss of BAS1 abolished or significantly reduced the repression of these genes in response to glycine removal but this phenotype was much less apparent in the absence of BAS2 or GCN4. Addition of a Bas1p-LexA fusion protein to a strain with a LexAop-LacZ fusion showed a strong glycine effect both in a BAS2 and a bas2 background. A Bas1p-VP16 fusion protein activated expression in a bas1bas2 strain but no glycine effect was observed while a Bas1p-Bas2p fusion protein activated expression to a lesser extent with a slight stimulation by glycine. These results suggest that glycine affects Bas1p activation of transcription rather than DNA binding and that Bas2p is not required for this affect. Glycine withdrawal repressed many of the same genes as addition of adenine, a process known to be dependent on Bas1p. However, the glycine response is independent of adenine repression, because glycine regulation occurs normally in ade strains. We did not see any difference in the degree of stimulation by glycine in the presence or absence of adenine even in Ade+ strains. Glycine regulation was also found to be dependent on an intact SHM2 gene, which encodes cytoplasmic serine hydroxymethyltransferase. A reporter plasmid containing a DNA sequence from the GCV2 promoter which confers glycine regulation on heterologous genes was introduced into the yeast deletion set to screen for genes required for glycine regulation. A number of genes, including BAS1 were required for activation by glycine but only the SHM2 gene was required for repression in the absence of glycine. We also showed that regulation of the SHM2 promoter by glycine requires Bas1p but not Bas2p or Gcn4p using a beta-galactosidase reporter. The response of the promoter to glycine required an intact SHM2 gene but was restored in a shm2 strain by addition of formate to the medium.

Adenine↗

PubMed1987

Substrate specificity of 3-methyladenine-DNA glycosylase from calf thymus.

3-Methyladenine-DNA glycosylase from calf thymus recognizes both 3-methyladenine (3-mAde), 7-methylguanine (7-mGua) and 3-methylguanine (3-mGua) residues in calf thymus DNA; the rate of release of 3-mAde is approximately eightfold higher than that for 7-mGua. The best DNA polymer substrates appeared to be those having an A-type helical conformation such as d(A-T)n and d(G-C)n. The Km values for release of 3-mAde and 7-mGua were approximately the same for the above mentioned two substrates whereas the Vmax for excision of 3-mAde was threefold higher than that of 7-mGua. The rate of hydrolysis of 7-mGua residues in d(G-C)n was similar to that found for the excision of 3-mAde in calf thymus DNA. The polymer d(G)n X d(C)m, which possesses a B-type helical conformation, was a poor substrate and the rate of excision here was approximately the same as with calf thymus DNA having the B-type structure. Polyamines greatly influenced the activity and at low concentrations a 50-100% increase in the release of 7-mGua, but not 3-mAde, was observed. With higher concentrations the rate of excision of both bases decreased sharply. The sequence specificity of the DNA glycosylase on naturally occurring DNA was studied using methylated DNA fragments from the plasmid pUC18. The results revealed that some 3-mAde as well as 7-mGua residues were seldom attacked. These 3-mAde residues were positioned either 5' to another Ade residue or in a stretch of pyrimidines, and the 7-mGua residue 3' to another Gua residue. The 3-mAde residue most frequently recognized was situated 3' to another Ade residue, and in the case of 7-mGua it was the central Gua residue in the sequence -G-G-G-.

Animals↗

PubMed2004

Patterns of self-cutting: a preliminary study on differences in clinical implications between wrist- and arm-cutting using a Japanese juvenile detention center sample.

The present study was aimed to clarify the differences in clinical implications between wrist- and arm-cutting. Subjects were 201 delinquent adolescents (178 males and 23 females) who had been admitted to a detention center from February to March 2003. A self-reporting questionnaire and the Adolescent Dissociative Experience Scale (ADES) were given. Traumatic events and other self-injurious behavior were compared among four groups. In total, 33 (16.4%) subjects reported wrist- and/or arm-cutting. Of the females, 60.9% (n = 14) had experienced self cutting behaviors compared to 10.7% of males (n = 19). Subjects were divided into four groups; 'non-cutting' (NC: n = 168, 83.6%), 'wrist-cutting' (WC: n = 5, 2.5%), 'arm-cutting' (AC: n = 19, 9.5%), and 'wrist- and arm-cutting' (WAC: n = 9, 4.5%). WC, AC, and WAC groups reported early separation, bulling in school, and histories of sexual/physical abuse more frequently than NC group. WC and WAC groups reported suicidal ideation and suicide attempts more frequently than NC and AC groups. The ADES scores in AC and WAC groups were significantly higher than in those in NC group (P < 0.001), while the scores in WC were not different from NC groups. WC and WAC groups self-cut due to suicide idea more frequently than the AC group, while AC group self-cut due to anger expression more frequently than WC or WAC groups. Self-cutters experienced early separation, bullying in school, and sexual/physical abuse more frequently than-non-self-cutters. Arm-cutting behavior may predict dissociation, while wrist-cutting may involve with suicidality.

Adolescent↗

PubMed2000

Inadvertent administration of sufentanil instead of fentanyl during sedation/analgesia in a community hospital emergency department: a report of two cases.

The authors report two cases of inadvertent administration of sufentanil instead of fentanyl during patient sedation/analgesia in a community hospital emergency department (ED). Both cases resulted in reversible adverse drug events (ADEs) to the respective patients. In tracing the steps involved in the cause of these errors, the authors discovered several components common to identified pathways that result in ADEs. These include similarities in product packaging appearance and names of these two medications, along with nursing unfamiliarity with the medications. Medication "sound-alikes" and "look-alikes" continue to be a source of potential error in the ED.

Accidents, Traffic↗

PubMed2006

Identification and classification of genes required for tolerance to high-sucrose stress revealed by genome-wide screening of Saccharomyces cerevisiae.

Yeasts used in bread making are exposed to high concentrations of sucrose during sweet dough fermentation. Despite its importance, tolerance to high-sucrose stress is poorly understood at the gene level. To clarify the genes required for tolerance to high-sucrose stress, genome-wide screening was undertaken using the complete deletion strain collection of diploid Saccharomyces cerevisiae. The screening identified 273 deletions that yielded high sucrose sensitivity, approximately 20 of which were previously uncharacterized. These 273 deleted genes were classified based on their cellular function and localization of their gene products. Cross-sensitivity of the high-sucrose-sensitive mutants to high concentrations of NaCl and sorbitol was studied. Among the 273 sucrose-sensitive deletion mutants, 269 showed cross-sensitivities to sorbitol or NaCl, and four (i.e. ade5,7, ade6, ade8, and pde2) were specifically sensitive to high sucrose. The general stress response pathways via high-osmolarity glycerol and stress response element pathways and the function of the invertase in the ade mutants were similar to those in the wild-type strain. In the presence of high-sucrose stress, intracellular contents of ATP in ade mutants were at least twofold lower than that of the wild-type cells, suggesting that depletion of ATP is a factor in sensitivity to high-sucrose stress. The genes identified in this study might be important for tolerance to high-sucrose stress, and therefore should be target genes in future research into molecular modification for breeding of yeast tolerant to high-sucrose stress.

Adaptation, Physiological↗

PubMed2004

Nitric oxide inhibits matrix metalloproteinase-2 expression via the induction of activating transcription factor 3 in endothelial cells.

Nitric oxide (NO) has been shown to inhibit migration of cells in which various matrix metalloproteinases (MMPs) are involved. The underlying molecular mechanisms of this inhibition remain elusive. Endothelial cells (ECs) constitutively produce MMP-2. The effect of NO on MMP-2 expression was examined. A dose-dependent inhibition of MMP-2 mRNA level was demonstrated in ECs treated with NO. ECs infected with adenovirus carrying endothelial NO synthase (Ade-NOS) reduced MMP-2 expression. The inhibitory effect of NO on MMP-2 expression was a transcriptional event because NO reduced MMP-2 promoter activity. NO treatment of ECs consequently suppressed MMP-2 secretion revealed by zymographic assay. Functional analysis of MMP-2 promoter (1716 base pairs) indicated that the p53-binding site (-1659 to -1629) was crucial for MMP-2 promoter activity. Activating transcription factor 3 (ATF3) has been reported to act as a transcriptional repressor for p53. ECs treated with NO induced ATF3 expression. Consistently, Ade-NOS-infected ECs showed an increase of ATF3 level. Moreover, ECs either over-expressed ATF3 or, when treated with an ATF3 activator (MG-132; carbobenzoxy-l-leucyl-l-leucyl-l-leucinal), resulted in a repression of MMP-2 promoter activity. Because of MMP-2 suppression by NO, ECs treated with NO inhibited endothelial migration, a phenomenon similar to that of ECs treated with MMP-2 antibody or MG-132. These results indicate that NO-attenuating endothelial migration is mediated at least in part by its reduction of MMP-2 expression via the up-regulation of ATF3. This study provides a molecular basis that supports the notion that NO acts as a negative regulator in endothelial migration.

Activating Transcription Factor 3↗

PubMed1980

Acceptance by Erwinia spp. of R plasmid R68.45 and its ability to mobilize the chromosome of Erwinia chrysanthemi.

R plasmid R68.45 was transferred in broth matings from Escherichia coli to strains of Erwinia amylovora, E. carotovora subsp. atroseptica, E. chrysanthemi, and E. herbicola (Enterobacter agglomerans); the frequency of transfer ranged from 2 x 10(-8) to 5 x 10(-4) per input donor cell depending on the bacterial species. The drug resistance markers tet(+), amp(+), and kan(+) were stable in these Erwinia species. Transconjugants of Erwinia spp., but not of the wild-type parent Erwinia strains, acquired levels of antibiotic resistance (tetracycline, 50 mug/ml; ampicillin, 200 mug/ml; kanamycin 200 mug/ml) similar to those of the donor R68.45-bearing strain of Escherichia coli. Erwinia transconjugants (with one exception of E. carotovora subsp. atroseptica) were donors of the antibiotic resistance markers; the frequency of transfer was consistently higher with an E. coli strain than with Erwinia spp. as recipients, and when matings were done on a solid surface (membranes) rather than in liquid. Transfer of chromosomal markers ade(+), gal(+), gtu(+) (utilization of galacturonate), his(+), leu(+), lys(+), thr(+), and trp(+) occurred in crosses between E. chrysanthemi strains harboring R68.45 and appropriate recipient strains; the frequency of transfer ranged from 9.0 x 10(-8) to 2.0 x 10(-6) depending on the selective marker. Analysis of the coinheritance of unselected markers among various classes of recombinants revealed linkage between thr-leu-lys-ade and between trp and his, thus confirming earlier findings with the Hfr-type donor cells. Since R68.45 mobilized an array of chromosomal markers in the wild-type as well as genetically marked strains of E. chrysanthemi, the system, used in conjunction with the existing Hfr strains, should provide a useful tool to study the genetics of plant pathogenicity of this bacterial species. In contrast to E. chrysanthemi, R68.45 did not mobilize chromosomal markers ilv(+), his(+), rbs(+), ser(+), and thr(+) in E. amylovora EA178.

Ampicillin↗

PubMed1982

Recombination analysis of naturally diploid Candida albicans.

A multiply auxotrophic strain, hOG45, was derived from Candida albicans ATCC 10261. Prototrophic revertants of this multiple auxotroph were selected after mutagenesis. These prototrophic revertants were distinguishable from the original prototroph, ATCC 10261, because of their mitotic instability. They gave rise to auxotrophic derivatives which displayed one or more of the auxotrophic requirements characteristic of hOG45. Two of the auxotrophic requirements, those for adenine and methionine, frequently reappeared together in the auxotrophic derivatives of the prototrophic revertants. This apparent linkage of ade and met was confirmed by protoplast fusion analysis of the original auxotroph. These data indicate that C. albicans ATCC 10261 is diploid, the multiple auxotroph h0G45 is homozygous for recessive auxotrophic alleles, the prototrophic revertants are multiple heterozygotes, the auxotrophic derivatives are homozygotes produced by mitotic crossing-over, and the association between the ade and met alleles is due to linkage.

Adenine↗

PubMed1968

Initiation of deoxyribonucleic acid synthesis after thymine starvation of Bacillus subtilis.

Evidence for premature initiation of deoxyribonucleic acid (DNA) replication after thymine starvation of Bacillus subtilis W23T(-) is presented, based on (i) increase in the number of ade(+) relative to met(+) transformants yielded by the DNA isolated from cultures after starvation (the ade(-) marker being near the origin of replication, whereas met(-) is close to the terminus), and (ii) increase in both the initial rate and final level of tritiated thymine incorporation in the presence of chloramphenicol after release from starvation. The marker ratio data agree quantitatively with the hypothesis that the initiation is induced only on one arm of each chromosome which was replicating prior to starvation.

Bacillus subtilis↗

PubMed1969

Defective bacteriophage PBSH in Bacillus subtilis. II. Intracellular development of the induced prophage.

Treatment of Bacillus subtilis strain 168 with mitomycin C caused induction of a defective prophage, PBSH. During induction, extensive deoxyribonucleic acid (DNA) synthesis took place. Concurrently, a change in marker frequency of the bacterial DNA was noticed. The frequency of only one marker, ade-16, the marker closest to the origin of the bacterial chromosome, was enhanced manyfold. DNA from whole phage particles transformed all bacterial markers at a frequency equal to that of DNA in the noninduced culture, except ade-16, the frequency of which was enhanced 30 to 100 times. Analysis of a double isotope experiment demonstrated that 14% of the phage DNA was derived from preinduction bacterial DNA. The other 86% of DNA in phage particles was DNA replicated after induction. Density label experiments with 5-bromodeoxyuridine showed that postinduction DNA synthesis took place preferentially at the origin region of the bacterial chromosome. Measurement of the molecular weight of DNA replicated after induction clearly showed that postinduction DNA replication is chromosomal. No evidence for prophage detachment and autonomous phage DNA replication was found. The data indicated that, after mitomycin C action, the bacterial chromosome under-went multiple reinitiation at the origin, while normal sequential DNA replication was stopped. The pool of replicated bacterial DNA was fragmented randomly. This DNA was packaged into PBSH particles which were released after cell lysis.

Bacillus subtilis↗

PubMed1990

Antibody-dependent enhancement of simian immunodeficiency virus (SIV) infection in vitro by plasma from SIV-infected rhesus macaques.

Plasma from two rhesus macaques (Macaca mulatta) experimentally infected with the simian immunodeficiency virus (SIV; isolate SIVmac251) enhanced SIVmac infection of a human CD4+ lymphoblastoid cell line, MT-2. Prechallenge plasma samples from these animals and serum from SIV-negative macaques did not enhance infection. Compared with controls, infection enhancement was characterized by the rapid appearance of syncytium formation (3 to 4 days sooner), reverse transcriptase release (10-fold increase), and cytopathic effect (60% cell killing). Enhancement of activity was dependent on the presence of diluted, fresh SIV-negative macaque serum as a source of complement. A requirement for complement was shown by the absence of enhancement in heat-inactivated serum and by dose-dependent inhibition of enhancement in the presence of polyclonal antibody to monkey complement component C3. Monoclonal antibody to CD4 (OKT4a) blocked enhancement completely, while monoclonal antibody to the human complement component C3d receptor CR2 (OKB7) reduced enhancement by greater than 50%, indicating a requirement for CD4 and CR2 in mediating this phenomenon. SIV infection-enhancing activity appeared in macaques soon after experimental inoculation (28 days). The titer increased over time and peaked just prior to the death of both macaques from opportunistic infections and lymphoma. In vitro SIV infection enhancement is nearly identical to the in vitro complement-mediated, antibody-dependent enhancing (C'-ADE) activity observed in human immunodeficiency virus-positive human sera (Robinson et al., Lancet i:790-794, 1988; Robinson et al., J. Acq. Immun. Def. Synd. 2:33-42, 1989). These observations validate the macaque-SIV model for studies of C'-ADE.

Animals↗

PubMed1990

Antibodies to the primary immunodominant domain of human immunodeficiency virus type 1 (HIV-1) glycoprotein gp41 enhance HIV-1 infection in vitro.

Previous experiments had shown that two human monoclonal antibodies (huMAbs) directed against human immunodeficiency virus type 1 (HIV-1) enhanced HIV-1 infection in vitro (Robinson et al., Proc. Natl. Acad. Sci. USA, 87:3185-3189, 1990). This complement-mediated, antibody-dependent enhancement (C'-ADE) of HIV-1 infection caused 12-fold increases in reverse transcriptase released from MT-2 cells. In the study reported here, it was demonstrated that both of these huMAbs, 86 and V10-9, bound to an immunodominant peptide in gp41 (amino acids 586 to 620). This peptide blocked C'-ADE of HIV-1 infection in vitro regardless of whether huMAb 86 or human polyclonal anti-HIV was used as the source of anti-HIV antibody. Blockade of enhanced infections was characterized by decreases in antigen synthesis, cytopathic effect, and reverse transcriptase release. The ability of the huMAbs to enhance infection was determined to be dependent upon specific peptide reactivity and not dependent upon immunoglobulin subclass, complement fixation, or gross antigen reactivity. Since the peptide to which enhancing antibodies bind is immunodominant and does not bind neutralizing antibodies, it may be worthwhile to investigate deletion of this 35-amino-acid peptide from candidate anti-HIV vaccines.

Amino Acid Sequence↗

PubMed1995

Increased adhesion as a mechanism of antibody-dependent and antibody-independent complement-mediated enhancement of human immunodeficiency virus infection.

Enhancement of human immunodeficiency virus (HIV) infection by complement alone or in conjunction with antibodies was studied experimentally and theoretically. Experimental studies showed that while HIV-positive sera neutralize HIV infection, the addition of fresh complement abrogated neutralization and could even cause enhancement. Enhancement was blocked by anti-complement receptor 2 antibodies, and infection under enhancing conditions could be blocked by soluble CD4. Antibody-dependent complement-mediated enhancement (C'ADE) was dependent on the alternative complement activation pathway, as factor B-deficient serum could enhance only after the addition of factor B. The observed enhancement was also antibody dependent, since the addition of antibodies increased the level of enhancement. Under C'ADE conditions, infection reached a plateau within 5 min and was not caused by activation of cells by factors in the human serum. On the contrary, preincubation of cells with complement decreased the level of enhancement. A theoretical model of HIV infection in vitro which exhibited similar enhancement in an antibody- and complement concentration-dependent way was developed. Model studies indicated that the enhanced infection process could be explained by the fact that virions, because of complement deposition on the surface, bind more efficiently to cells. The model also indicated that the saturation of the enhanced infection process seen after a few minutes could be caused by saturation of the complement receptors. The effect of neutralizing antibodies can thus be overcome by the enhancing effect of complement that facilitates the contact between gp120 and CD4. These studies demonstrate that the main features of the complement-dependent enhancement phenomenon can be understood in terms of a simple mathematical model.

CD4 Antigens↗

PubMed1993

Epigenetic switching of transcriptional states: cis- and trans-acting factors affecting establishment of silencing at the HMR locus in Saccharomyces cerevisiae.

In this study, we used the ADE2 gene in a colony color assay to monitor transcription from the normally silent HMR mating-type locus in Saccharomyces cerevisiae. This sensitive assay reveals that some previously identified cis- and trans-acting mutations destabilize silencing, causing genetically identical cells to switch between repressed and derepressed transcriptional states. Deletion of the autonomously replicating sequence (ARS) consensus element at the HMR-E silencer or mutation of the silencer binding protein RAP1 (rap1s) results in the presence of large sectors within individual colonies of both repressed (Ade-, pink) and derepressed (Ade+, white) cells. These results suggest that both the ARS consensus element and the RAP1 protein play a role in the establishment of repression at HMR. In diploid cells, the two copies of HMR appear to behave identically, suggesting that the switching event, though apparently stochastic, reflects some property of the cell rather than a specific event at each HMR locus. In the ADE2 assay system, silencing depends completely upon the function of the SIR genes, known trans-acting regulators of the silent loci, and is sensitive to the gene dosage of two SIR genes, SIR1 and SIR4. Using the ADE2 colony color assay in a genetic screen for suppressors of rap1s, silencer ARS element deletion double mutants, we have identified a large number of genes that may affect the establishment of repression at the HMR silent mating-type locus.

Cloning, Molecular↗

PubMed1999

Is the growth of brown adipocytes necessary for cold acclimation in mice?

Chronic exposure to cold increases the growth of brown adipose tissue and the resistance to more severe cold, thus improving thermogenesis. The present study examined the possibility that dietary compounds can modify cold acclimation. Adenosine (ADO) or adenine (ADE) were administered in drinking water (0.05%, w/v) for 5 weeks to male ddY strain mice from 4 weeks of age. At 5 weeks of age, the mice were exposed to 4 degrees C for 4 weeks. After termination of this period, the interscapular brown adipose tissue (IBAT) and rectal temperature on acute exposure to severe cold (-20 degrees C) for 60 min were measured. Chronic exposure to cold increased the weight of IBAT and made mice resistant to a fall in rectal temperature on exposure to severe cold. The growth of IBAT and improvement in thermogenesis can be used as a cold acclimation profile in ddY mice. The growth of IBAT was selectively prevented by ingestion of ADO. The improvement in thermogenesis was reduced, but only a little, by the ingestion of either ADO or ADE. Thus, growth of brown adipocytes might not be necessary for cold acclimation in mice.

Acclimatization↗