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PubMed2005

Stability of EcoRI restriction-modification enzymes in vivo differentiates the EcoRI restriction-modification system from other postsegregational cell killing systems.

Certain type II restriction modification gene systems can kill host cells when these gene systems are eliminated from the host cells. Such ability to cause postsegregational killing of host cells is the feature of bacterial addiction modules, each of which consists of toxin and antitoxin genes. With these addiction modules, the differential stability of toxin and antitoxin molecules in cells plays an essential role in the execution of postsegregational killing. We here examined in vivo stability of the EcoRI restriction enzyme (toxin) and modification enzyme (antitoxin), the gene system of which has previously been shown to cause postsegregational host killing in Escherichia coli. Using two different methods, namely, quantitative Western blot analysis and pulse-chase immunoprecipitation analysis, we demonstrated that both the EcoRI restriction enzyme and modification enzyme are as stable as bulk cellular proteins and that there is no marked difference in their stability. The numbers of EcoRI restriction and modification enzyme molecules present in a host cell during the steady-state growth were estimated. We monitored changes in cellular levels of the EcoRI restriction and modification enzymes during the postsegregational killing. Results from these analyses together suggest that the EcoRI gene system does not rely on differential stability between the toxin and the antitoxin molecules for execution of postsegregational cell killing. Our results provide insights into the mechanism of postsegregational killing by restriction-modification systems, which seems to be distinct from mechanisms of postsegregational killing by other bacterial addiction modules.

Deoxyribonuclease EcoRI↗

PubMed1988

Dietary restriction and presbyacusis: periods of restriction and auditory threshold losses in the CBA/J mouse.

Dietary restriction was imposed on CBA/J mice, animals which develop presbyacusis late in their lives. Animals restricted for their whole lives, as well as those restricted after midlife, had less presbyacusis than did control mice fed ad libitum. Dietary restriction did not increase the life spans of these mice. Restriction until midlife did not protect from presbyacusis, nor did it increase life span. In this genotype, dietary restriction protects against hearing loss only if it occurs at the age of most rapid decline of cochlear function.

Aging↗

PubMed1984

Abdominal fat deposition and sudden death syndrome in broilers: the effects of restricted intake, early life caloric (fat) restriction, and calorie: protein ratio.

The effects of feed restriction, early life fat restriction, and calorie:protein ratio on abdominal fat pad development and sudden death syndrome (SDS) in the broiler chicken were studied in two experiments. In Experiment 1, restricting feed intake to 90% of ad libitum intake was found to reduce significantly (P less than .01) both 49-day body weights and abdominal fat pad size while feed efficiency was significantly (P less than .01) improved compared to groups fed a wheat diet ad libitum. Corn-fed birds tended to outperform wheat fed groups. Reduced growth rate or supplementation of the diet with additional vitamins and minerals did not effect the incidence of SDS. In Experiment 2, fat restriction in the diet from 0 to 7 days initially reduced growth rate and increased feed:gain ratios. By 49 days, no effect of fat restriction on these parameters was observed. Dietary fat restriction tended to increase abdominal fat measured at 49 days of age. Lowering the calorie: protein ratio of the finishing diet significantly (P less than .05) improved feed:gain ratios measured from 29 to 49 days and tended to reduce fat pad size. Incidence of SDS was significantly (P less than .05) lower from 29 to 56 days in groups fed the 24% protein finisher diet as compared to birds fed a 19% finisher diet.

Abdomen↗

PubMed1992

Restricted feeding and broiler performance: age at initiation and length of restriction.

Broiler cockerels were provided either ad libitum access or restricted to alternate-day access to feed initiated at different ages and lasting for different durations. Regimens consisted of ad libitum feeding; alternate-day feeding; alternate-day feeding from 0 to 6, 6 to 12, or 12 to 18 days of age (DOA); alternate-day feeding from 0 to 12, 0 to 6, and 12 to 18, or 6 to 18 DOA; and alternate-day feeding from 0 to 18 DOA. By 39 DOA, chicks restricted for only one 6-day period reached body weights equivalent to those of chicks eating ad libitum. Body weights of chicks restricted for more than 6 days during the first 18 days after hatch were lower than those of chicks eating ad libitum at 39 DOA. Restriction for more than 6 days improved feed efficiency. Chicks restricted for the whole experiment had superior feed efficiency but low body weights. Antibody responses to sheep erythrocyte antigen were similar among feeding regimens. Response to Escherichia coli inoculation was generally less severe in chicks provided restricted access to feed, and overall mortality was highest in chicks eating ad libitum. Feeding regimens had little effect on organ weights relative to body weight, amount of abdominal fat (either on an absolute basis or relative to body weight), or percentage lipid in the abdominal fat pad.

Abdomen↗

PubMed1994

Non-steroidal anti-inflammatory drugs: restrictive or non-restrictive hepatic clearance?

Based on their hepatic extraction ratio and unbound fraction in plasma or blood, drugs can be categorized as being restrictively or non-restrictively eliminated. The general perception is that drugs with very small plasma clearances and extensive plasma protein binding, such as warfarin, are eliminated restrictively. However, based on literature data for 18 non-steroidal anti-inflammatory drugs (NSAIDs) with low plasma clearances (< 60 ml/min), we have shown that most of these low-extraction compounds are non-restrictively eliminated, i.e. their hepatic extraction ratio exceeds their unbound fraction in plasma. For 4 NSAIDs considered in this survey, i.e. phenylbutazone and the oxicams piroxicam, isoxicam and tenoxicam, the hepatic extraction ratio is smaller than their unbound fraction in plasma, and their hepatic elimination, therefore, is restrictive. Our conclusion that most low-clearance NSAIDs are non-restrictively extracted is based on a number of realistic assumptions concerning their pharmacokinetic characteristics: 1. their elimination is exclusively hepatic, 2. bioavailability of their oral dosage form is complete, and 3. they do not undergo extensive reversible biotransformation or enterohepatic circulation.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1985

A fine restriction map of the linear mitochondrial DNA of Tetrahymena pyriformis: genome size, map locations of rRNA and tRNA genes, terminal inversion repeat, and restriction site polymorphism.

A fine restriction map of the linear mitochondrial DNA of Tetrahymena pyriformis strain ST is presented. 1. Based on agarose gel electrophoresis data together with limited nucleotide sequences available on some restriction fragments, we estimate the actual size of this genome to be about 55,000 base pairs. 2. Seven tRNA gene locations have been assigned, which are scattered along the genome length. Six of these locations encode the genes for tRNA(phe), tRNA(his), tRNA(trp), and tRNA(glu), and the duplicate tRNA(tyr) genes which are located at the inverted terminal repeat segments. The tRNA gene(s) encoded in one location has not been identified. We have not yet found the tRNA(leu) and tRNA(met) genes, which were previously shown to be encoded in the genome (Chiu et al. 1974; Suyama 1982). 3. We have mapped the 14S rRNA gene by sequencing the 170 bp segment of EcoRI fragment 8 and by aligning its sequence with E. coli 16S rRNA. From our recent complete sequence data the gene size was found to be about 1,650 bp, which is unexpectedly large for the 14S rRNA which has an estimated size of 1,300 bp. The 14S rRNA is probably a cleavage product of the larger primary transcript of which 200-300 bases of the 5' end are missing. 4. The duplicate copies of the 21S rRNA gene at the terminal duplication inversion segments were analyzed. ClaI fragment 7 (1,500 bp) corresponds in sequence from base position 850 to 2,390 of the 20S rRNA gene of Paramecium mitochondrial DNA (Seilhamer et al. 1984b). The 21S gene is approximately 2,500 bp long. The presence of some restriction site polymorphism is apparent in this segment. 5. Each of the 21S gene copies precedes the tRNA(tyr) gene, but the space flanking one tRNA(tyr) gene differs in size and restriction sites from the space flanking another tRNA(tyr) gene. Thus, this space corresponds to the segment of an imperfect match in the terminal duplication inversion of Goldbach et al. (1978a). 6. Saccharomyces cerevisiae mitochondrial probes including Cob, ATPase VI and IX, and cytochrome oxidase I gene sequences, 21S and 15S rRNAs, and mouse mitochondrial DNA showed no significant hybridization with any restriction fragments of Tetrahymena mitochondrial DNA. The results are in accordance with an extensive sequence divergence previously found in the Tetrahymena mitochondrial genome (Goldbach et al. 1977).

Animals↗

PubMed1983

Restriction of bacteriophage T3 and T7 ocr+ strains by the type II restriction endonuclease EcoRV.

When E. coli cells carrying the plasmid pLG13 (coding for the newly discovered type II restriction endonuclease EcoRV) are infected with phage T3 or T7, only T7 is able to replicate normally. T3 wild-type as well as its ocr- mutants are subject to DNA restriction in vivo and in vitro. The EcoRV enzyme cuts T3 DNA at 5 sites. T7 and its ocr- mutants have no EcoRV sites in their DNA. In contrast to the anti-restriction activity of the T3 and T7 ocr+ gene function against type I and III restriction enzymes, the ocr+ protein is unable to inactivate the type II restriction endonuclease EcoRV.

DNA Replication↗

PubMed2005

The biology of restriction and anti-restriction.

The phenomena of prokaryotic restriction and modification, as well as anti-restriction, were first discovered five decades ago but have yielded only gradually to rigorous analysis. Work presented at the 5th New England Biolabs Meeting on Restriction-Modification (available on REBASE, http://www.rebase.com) and several recently published genetic, biochemical and biophysical analyses indicate that these fields continue to contribute significantly to basic science. Recently, there have been several studies that have shed light on the still developing field of restriction-modification and on the newly re-emerging field of anti-restriction.

Bacteria↗

PubMed2001

Comparison of the effect of dietary fat restriction with that of energy restriction on human lipid metabolism.

BACKGROUND: Dietary fat and energy have been implicated as factors controlling circulating total and LDL-cholesterol concentrations. Whether these factors work independently or synergistically in regulating human cholesterol metabolism remains to be fully elucidated. OBJECTIVE: The objective was to determine whether the effects of fat restriction on circulating lipid concentrations and synthesis differ from those of energy restriction in hypercholesterolemic subjects fed controlled diets. DESIGN: Eleven men (LDL > 3.6 mmol/L) participated in a randomized crossover study. Subjects consumed 4 prepared diets, each for 4 wk and separated by 6 wk, that contained either typical amounts of fat and energy (TF), low amounts of fat but adequate energy (LF), low amounts of fat and energy through carbohydrate restriction (LFE), or typical amounts of fat and low energy through carbohydrate restriction (LE). RESULTS: Body weights declined (P < 0.001) after the LE and LFE diets. Total cholesterol concentrations were not significantly different between the diets. LDL cholesterol was lower (P < 0.05) after the LF and LFE diets (8.2% and 8.0%, respectively) than after the TF diet. The LE diet increased HDL cholesterol (46.8%) and decreased triacylglycerols (22.7%), whereas the LF diet increased triacylglycerols (23.6%), relative to the TF diet. LDL:HDL decreased after the LE and LFE diets (P < 0.05). Cholesterol fractional synthesis rates after the LF, LE, and LFE diets were lower (35.2%, 27.7%, and 25.5%, respectively; P < 0.05) relative to the TF diet. CONCLUSION: Reductions in both dietary fat and energy may modify LDL cholesterol by lowering cholesterol biosynthesis; however, the increase in HDL cholesterol and the suppression of triacylglycerol concentrations and LDL:HDL suggests that favorable plasma lipid profiles were also achieved through energy restriction alone.

Adult↗

PubMed1996

Localization of prophages of serological group B and F on restriction fragments defined in the restriction map of Staphylococcus aureus NCTC 8325.

Several Staphylococcus aureus strains were lysogenized by the phages of serological group B (phages phi 53, phi 85) as well as by some of serological group F (phages phi 77, phi 84) and macrorestriction fragment patterns of genomic DNA were estimated in the lysogenized, non-lysogenic and delysogenized (cured of prophages) strains. It was shown that the integration of phage DNA into chromosome of S. aureus leads to specific changes in restriction fragment pattern in all the lysogenized strains. These changes correlate well with the SmaI restriction map of S. aureus NCTC 8325 since they concern the restriction fragments defined in this map. Phages phi 53 and phi 85 integrate into SmaI fragment B. On the other hand, phages phi 77 and phi 84 integrate into SmaI fragment E of the S. aureus restriction map. The prophages of strain NCTC 8511 have their integration sites, as follows: the phage designated by us phi M integrates in fragment A, whereas the integration site for phage phi J lies in fragment E. Phage phi M was estimated to be genetically related to phages of serological group A and phage phi J to those of serological group F. Evidence was given that lysogenization of S. aureus strains by at least four prophages does not cast any doubt upon the estimation of their genetic relatedness based on their similarity in restriction pattern.

Attachment Sites, Microbiological↗

PubMed1999

REF Select: expert system software for selecting restriction endonucleases for restriction endonuclease fingerprinting.

REF Select, expert system software, has been developed to assist in the selection of optimal restriction endonucleases for restriction endonuclease fingerprinting (REF), a method for rapid and sensitive mutation screening of long DNA segments (1-2 kb). The REF method typically involves six separate digestions with up to two restriction endnonucleases used in each digestion. If done manually, performing a comprehensive review of the large number of possible sets of restriction endonucleases that could be used (over 10(19) in the example presented here) and making an optimal choice is not feasible. Furthermore, the typical nonoptimal manual selection takes approximately 8 h by someone experienced with REF. REF Select enables a comprehensive review of the possible sets and a consistent, objective and fast selection of an optimal set by using a two-step strategy: the selection of sets that meet specific constraints, which is followed by a ranking of those sets by an optimality score. Based on our experience with REF, we chose default selection and ranking parameters to help the user get started quickly. These parameters form a knowledge base that can be customized and then saved by the user. In conclusion, REF Select facilitates the general application of REF by serving as an expert system for the selection of optimal restriction endonucleases. We demonstrated REF Select using an example segment from the human p53 gene.

Algorithms↗

PubMed1995

Effects of a behavioral weight loss program stressing calorie restriction versus calorie plus fat restriction in obese individuals with NIDDM or a family history of diabetes.

OBJECTIVE: The aim of this randomized trial was to compare the effects of a behavioral intervention focusing on either calorie restriction alone or calorie plus fat restriction on weight loss and changes in lipids and glycemic control in individuals with non-insulin-dependent diabetes mellitus (NIDDM) or a family history of diabetes. RESEARCH DESIGN AND METHODS: We recruited 44 obese women with NIDDM and 46 obese women with a family history of NIDDM and randomly assigned these subjects to calorie restriction (CAL) or to calorie plus fat restriction (CAL + FAT). All subjects participated in a 16-week behavioral weight loss program, with training in diet, exercise, and behavior modification. Subjects assigned to the CAL condition were given a 1,000-1,500 kcal/day goal and self-monitored calories consumed. Subjects assigned to the CAL+FAT condition had the same calorie goal, but were also given a fat goal (grams of fat/day), to produce a diet with < 20% of calories from fat; this group monitored both calories and fat grams. RESULTS: Among NIDDM subjects, weight loss of the subjects in the CAL+FAT condition was significantly greater than subjects in the CAL condition (7.7 vs. 4.6 kg) and the CAL+FAT condition group also maintained their weight loss better at the 1-year follow-up (5.2 vs. 1.0 kg). Significant decreases in glucose, high-density lipoprotein (HDL) cholesterol, and total cholesterol were seen after 16 weeks of treatment among NIDDM subjects; these changes were similar in CAL and CAL+FAT groups, but a greater proportion of subjects in CAL condition required oral hypoglycemic medication. At the 1-year follow-up, all parameters had returned to baseline. No significant differences in weight loss or physiological changes were seen between CAL and CAL+FAT conditions in subjects with a family history of diabetes. CONCLUSIONS: These results suggest that using the combination of calorie and fat restriction may help promote weight loss in obese NIDDM patients. No other long-term benefits of this regimen were observed.

Behavior Therapy↗

PubMed2003

[Role of "anti-restriction" motif in functional activity of anti-restriction protein ArdA pKM101 (incN)].

A number of mutant forms of the antirestriction protein ArdA encoded by the ardA gene located in a transmissive IncN plasmid pKM101 have been constructed. Proteins belonging to the Ard family are specific inhibitors of type I restriction--modification enzymes. Single mutational substitutions of negatively charged amino acid residues located in the "antirestriction motif" with hydrophobic alanine, E134A, E137A, D144A, or a double substitution E134A, E137A do not affect the antirestriction activity (Ard) of ArdA but almost completely abolish the antimodification activity (Amd). Mutational substitutions F107D and A110D in the assumed interface ArdA, which determines contact between monomers in the active dimer (Ard)2, cause an approximately 100-fold decrease in the antirestriction protein activity. It is hypothesized that the ArdA protein forms two complexes with the type I restriction--modification enzyme (R2M2S): (1) with a specific region in the S subunit involved in contact with the sK site in DNA; and (2) with a nonspecific region in the R subunit involved in DNA translocation and degradation by restriction endonucleases. The association of ArdA with the specific region inhibits restriction endonuclease and methyltransferase activities simultaneously, whereas the association of ArdA with a nonspecific region inhibits only restriction endonuclease activity of the R2M2S enzyme.

Amino Acid Motifs↗

PubMed1988

[Effect of recB- and recA-mutations on phage restriction in various modification-restriction plasmid systems of E. coli].

The effect of recB and recA mutations on lambda vir and P1 vir restriction by different restriction-modification plasmid systems of E. coli was studied. It was shown that effect of R1 plasmid coded restriction-modification in E. coli K12 and E. coli B strains and pJA4620 plasmid coded restriction in E. coli K12 is observed only in RecB+ strain. Phenomenon of restriction-modification determined by R124, R245 plasmids does not depend of recB mutation. Effect of recA mutation has not been found in cultures harbouring R1, R245, R124 pJA4620 plasmids.

Coliphages↗

PubMed1976

A restriction endonuclease analysis of the bacterial plasmid controlling the ecoRI restriction and modification of DNA.

Genetic analyses of DNA restriction and modification mechanisms have been encumbered by the inability to rigorously select for mutant phenotypes associated with these systems. The application of restriction endonucleases has now proved to be a successful approach to the genetic analyses of small genomes that are recalcitrant to the more standard genetic techniques. Restriction endonucleases EcoRI and HindIII were used to analyze the structure of the plasmid genome responsible for the EcoRI restriction endonuclease and modification methylase. This plasmid in the original clinical isolate of Escherichia coli appears to be identical to the ColE 1 plasmid except for a 1.95 kilobase pair segment which contains these genes. A preliminary restriction map of this plasmid is presented.

Base Sequence↗

PubMed1988

Epitopes associated with major histocompatibility complex (MHC) restriction site of T cells. IV. I-J epitopes on MHC-restricted cloned T cells.

We studied the expression of an I-Jk epitope on class II-restricted cloned L3T4+ T cells established from H-2k, H-2b, F1 and semiallogeneic radiation bone marrow chimeras by the inhibition of antigen-induced T cell proliferation and in vitro secondary antibody response, and by the direct immunofluorescence with a monoclonal anti-I-Jk. Both I-Ak- and I-Ek-restricted T cells were shown to carry the identical I-Jk epitope regardless of their genotypic origins, antigen specificity, and helper or suppressor function. None of the I-Ab-restricted clones derived from similar animals showed the I-Jk epitope. This isomorphism, regardless of the restriction specificity for I-Ak or I-Ek, contradicts the idea that I-J is an idiotypic determinant on class II-restricted T cell antigen receptor (TcR). In fact, the I-Jk epitope was not comodulated with TcR/T3 complex when incubated with an anti-T3 antibody, indicating that I-J is a new isomorphic receptor for self different from TcR alpha/beta heterodimers.

Animals↗

PubMed1995

Formaldehyde inactivation of measles virus abolishes CD46-dependent presentation of nucleoprotein to murine class I-restricted CTLs but not to class II-restricted helper T cells.

To induce an MHC-restricted specific CTL or Th response, an antigen must be delivered into the appropriate cellular compartment. We explored the role of CD46 in the presentation of measles virus (MV) nucleoprotein (NP) to murine NP-specific and MHC Class I-restricted polyclonal CTLs and the effect of inactivating MV by uv or formaldehyde. CD46(-)- and CD46(+)-transfected murine cells were used as target cells. After MV infection, only the targets which expressed CD46 were lysed by NP-specific class I-restricted CTLs. When MV was uv-inactivated, NP presentation by MHC class I molecules was retained but could be blocked by fusion inhibitors which block virus cell entry. When MV was inactivated with formaldehyde, NP was no longer presented by MHC class I molecules, although it was still presented by MHC class II molecules to a NP-specific class II-restricted T cell hybridoma. These data show that MV binding to the CD46 molecule is a prerequisite for virus-to-cell fusion and that cytosolic delivery of NP is necessary for presentation by class I molecules. Moreover, formaldehyde inactivation of virus induces the loss of class I-restricted presentation of NP due to selective abrogation of fusion and cytosolic delivery of NP.

Amino Acid Sequence↗

PubMed2002

Restriction of a Sindbis virus mutant in BHK cells and relief of the restriction by the addition of adenosine.

SV(PZF) is a mutant of Sindbis virus (SV) which we selected on the basis of its ability to replicate in mosquito cells treated with pyrazofurin (PZF), a drug which inhibits pyrimidine nucleotide biosynthesis (Lin et al., 2000, Virology 272, 61-71). Three mutations, A6627U, A7543U, and C7593A, were identified in the nsP4 (the viral RNA polymerase) coding region, which were required for the PZF-resistant phenotype. We report here that SV(PZF) has a second phenotype. Its replication in BHK cells is severely restricted; yields of SV(PZF) from BHK cells are 100- to 1000-fold lower than the yields of standard SV (SV(STD)). However, addition of adenosine to the SV(PZF)-infected cultures completely relieves this restriction and results in yields comparable to those observed with SV(STD). Adenosine has no effect on the yield of SV(STD) from BHK cells. Synthesis of the viral structural proteins is markedly depressed in SV(PZF)-infected BHK cells, as is synthesis of the viral subgenomic (SG) RNA from which these proteins are translated. In contrast, normal amounts of genomic RNA are made. Experiments with mutagenized viruses indicated that the SV(PZF) mutation, C7593A, by itself, was sufficient to produce the restriction phenotype. However, this mutation not only changes Pro 609 of nsP4 to Thr, it also changes the nucleotide at the minus sign5 position of the SG promoter. To evaluate the relative contributions of the change in nsP4 and the change in the SG promoter to the restriction phenotype, we made use of double SG viruses, in which nsP4 and the promoter for the SG RNA which encodes the structural proteins can be changed independent of each other. Our results indicated that both the change in nsP4 and the change in the SG promoter were required to produce the full restriction phenotype. We suggest that the changes in nsP4 and the SG promoter destabilize the RNA initiation complex assembled at the SG promoter and that since ATP is the initiating nucleotide in the SG RNA transcript, the increased level of ATP resulting from the addition of adenosine is able to compensate for this destabilization and restore the synthesis of SG RNA to normal levels.

Adenosine↗