OMPwiki - User contributions [en]

PMID:369552

2012-08-30T15:28:44Z

165.91.108.7: New PMID: Page!

PMID:369552

2012-08-30T15:28:44Z

165.91.108.7: Fill PMID: Page!

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{| id="B503f86ac8099b" class=" tableEdit PMID_info_table"

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!align=left |Citation
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'''Giordano, G, Grillet, L, Rosset, R, Dou, JH, Azoulay, E and Haddock, BA''' (1978) Characterization of an Escherichia coli K12 mutant that is sensitive to chlorate when grown aerobically.''Biochem. J.'' '''176''':553-61
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!align=left |Abstract
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Escherichia coli can normally grow aerobically in the presence of chlorate; however, mutants can be isolated that can no longer grow under these conditions. We present here the biochemical characterization of one such mutant and show that the primary genetic lesion occurs in the ubiquinone-8-biosynthetic pathway. As a consequence of this, under aerobic growth conditions the mutant is apparently unable to synthesize formate dehydrogenase, but can synthesize a Benzyl Viologen-dependent nitrate reductase activity. The nature of this activity is discussed.
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!align=left |Links
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=369552 PubMed]

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!align=left |Keywords
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Acridines; Aerobiosis; Chlorates; Cytochromes; Escherichia coli; Formates; Mutation; NADP Transhydrogenases; Nitrate Reductases; Quinones; Spectrometry, Fluorescence

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==Main Points of the Paper ==
{{LitSignificance}}

== Materials and Methods Used ==
{{LitMaterials}}

==Phenotype Annotations==
{{AnnotationTableHelp}}
<protect>

{| id="T503f86ac83737" class=" tableEdit Phenotype_Table_2"
|-
!|Phenotype of!!Taxon Information!!Genotype Information (if known)!!Condition Information!!OMP ID!!OMP Term Name!!ECO ID!!ECO Term Name!!Notes!!Status

|- class="tableEdit_footer"
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|}
</protect>

==Notes==

==References==
{{RefHelp}}
<references/>

[[Category:Publication]]

PMID:4942764

2012-08-30T15:26:50Z

165.91.108.7: Fill PMID: Page!

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{| id="O503f8639e19d8" class=" tableEdit PMID_info_table"

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!align=left |Citation
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'''Russell, RR and Pittard, AJ''' (1971) Mutants of Escherichia coli unable to make protein at 42 C.''J. Bacteriol.'' '''108''':790-8
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!align=left |Abstract
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Members of a collection of mutants of Escherichia coli unable to form colonies on nutrient agar at 42 C have been characterized on the basis of their growth response to a shift from 32 to 42 C in liquid medium. Forty-four mutants, which show an abrupt, nonlethal cessation of growth when moved to the restrictive temperature, have been characterized with respect to the effect of the mutation responsible for temperature sensitivity on deoxyribonucleic acid, ribonucleic acid, and protein synthesis. In 12 mutants, the mutation causing temperature sensitivity of growth primarily affects protein synthesis, in each case through an altered aminoacyl-transfer ribonucleic acid synthetase. Mutants with temperature-sensitive glutamyl-, phenylalanyl-, and valyl-transfer ribonucleic acid synthetases have been obtained, and the genes specifying these enzymes have been mapped by conjugation and transduction. Another mutant has been shown to possess a temperature-sensitive tryptophanyl-transfer ribonucleic acid synthetase, but this is not responsible for inability to grow at 42 C on media containing tryptophan.
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!align=left |Links
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=4942764 PubMed]

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!align=left |Keywords
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Agar; Amino Acyl-tRNA Synthetases; Bacterial Proteins; Carbon Isotopes; Cell-Free System; Chromosome Mapping; Conjugation, Genetic; Culture Media; DNA, Bacterial; Escherichia coli; Genes; Glutamates; Hot Temperature; Leucine; Mutagens; Mutation; Nitrosoguanidines; Phenylalanine; RNA, Bacterial; Thymidine; Transduction, Genetic; Tritium; Uracil; Valine

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|}


==Main Points of the Paper ==
{{LitSignificance}}

== Materials and Methods Used ==
{{LitMaterials}}

==Phenotype Annotations==
{{AnnotationTableHelp}}
<protect>

{| id="P503f8639e3d4f" class=" tableEdit Phenotype_Table_2"
|-
!|Phenotype of!!Taxon Information!!Genotype Information (if known)!!Condition Information!!OMP ID!!OMP Term Name!!ECO ID!!ECO Term Name!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.3275.P503f8639e3d4f&page=3275&pagename={{FULLPAGENAMEE}}&type=0&template=Phenotype_Table_2 edit table] || || || || || || || || ||
|}
</protect>

==Notes==

==References==
{{RefHelp}}
<references/>

[[Category:Publication]]

PMID:4942764

2012-08-30T15:26:49Z

165.91.108.7: New PMID: Page!

PMID:2191080

2012-08-30T15:25:15Z

165.91.108.7: New PMID: Page!

PMID:2191080

2012-08-30T15:25:15Z

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{| id="I503f85db967ee" class=" tableEdit PMID_info_table"

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'''Birch, RG, Pemberton, JM and Basnayake, WV''' (1990) Stable albicidin resistance in Escherichia coli involves an altered outer-membrane nucleoside uptake system.''J. Gen. Microbiol.'' '''136''':51-8
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!align=left |Abstract
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Albicidin blocked DNA synthesis in intact cells of a PolA- EndA- Escherichia coli strain, and in permeabilized cells supplied with all necessary precursor nucleotides, indicating a direct effect on prokaryote DNA replication. Replication of phages T4 and T7 was also blocked by albicidin in albicidin-sensitive (Albs) but not in albicidin-resistant (Albr) E. coli host-cells. All stable spontaneous Albr mutants of E. coli simultaneously became resistant to phage T6. The locus determining albicidin sensitivity mapped at tsx, the structural gene for an outer-membrane protein used as a receptor by phage T6 and involved in transport through the outer membrane of nucleosides present at submicromolar extracellular concentrations. Albicidin does not closely resemble a nucleoside in structure. However, Albs E. coli strains rapidly accumulated both nucleosides and albicidin from the surrounding medium whereas the Albr mutants were defective in uptake of nucleosides and albicidin at low extracellular concentrations. An insertion mutation blocking Tsx protein production also blocked albicidin uptake and conveyed albicidin resistance. Albicidin supplied at approximately 0.1 microM blocked DNA replication within seconds in intact Albs E. coli cells, but a 100-fold higher albicidin concentration was necessary for a rapid inhibition of DNA replication in permeabilized cells. We conclude that albicidin is effective at very low concentrations against E. coli because it is rapidly concentrated within cells by illicit transport through the tsx-encoded outer-membrane channel normally involved in nucleoside uptake. Albicidin resistance results from loss of the mechanism of albicidin transport through the outer membrane.
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!align=left |Links
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2191080 PubMed]

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!align=left |Keywords
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Anti-Bacterial Agents; Cell Membrane; Chromosome Mapping; Dose-Response Relationship, Drug; Drug Resistance, Microbial; Escherichia coli; Mutation; Nucleosides; Organic Chemicals; Xanthomonas

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.3274.I503f85db967ee&page=3274&pagename={{FULLPAGENAMEE}}&type=1&template=PMID_info_table edit table] ||
|}


==Main Points of the Paper ==
{{LitSignificance}}

== Materials and Methods Used ==
{{LitMaterials}}

==Phenotype Annotations==
{{AnnotationTableHelp}}
<protect>

{| id="P503f85db9c2af" class=" tableEdit Phenotype_Table_2"
|-
!|Phenotype of!!Taxon Information!!Genotype Information (if known)!!Condition Information!!OMP ID!!OMP Term Name!!ECO ID!!ECO Term Name!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.3274.P503f85db9c2af&page=3274&pagename={{FULLPAGENAMEE}}&type=0&template=Phenotype_Table_2 edit table] || || || || || || || || ||
|}
</protect>

==Notes==

==References==
{{RefHelp}}
<references/>

[[Category:Publication]]

PMID:783128

2012-04-26T17:22:54Z

165.91.108.7: Fill PMID: Page!

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{| id="E4f99846dd718c" class=" tableEdit PMID_info_table"

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!align=left |Citation
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'''Manning, PA and Reeves, P''' (1976) Outer membrane of Escherichia coli K-12: differentiation of proteins 3A and 3B on acrylamide gels and further characterization of con (tolG) mutants.''J. Bacteriol.'' '''127''':1070-9
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!align=left |Abstract
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Two classes of mutants, con and tolG, that appeared to be very similar in a number of respects have been shown to be identical and cotransducible with pyrD. By diethylaminoethyl-cellulose chromatography of the outer membranes, we have shown that the mutants are missing only protein 3A and retain protein 3B. Using con mutants, we were thus able to identify protein 3B on the pH 7.2 gel system of Maizel where it runs separately from protein 3A if unheated samples are used. tolG mutants were shown to be identical to con mutants in being conjugation defective with most F-like plasmid donors but not with I-like plasmid donors, and in their resistance pattern to bacteriophages and colicins. During the course of this study, it was observed that the bacteriocin produced by Serratia marcescenc JF246 was identical in its activity spectrum to colicin L-398 and is now considered to be a colicin of type L.
|-
!align=left |Links
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=783128 PubMed]

|-
!align=left |Keywords
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Anti-Bacterial Agents; Bacterial Proteins; Cell Membrane; Chromosome Mapping; Chromosomes, Bacterial; Colicins; Coliphages; Drug Resistance, Microbial; Electrophoresis, Polyacrylamide Gel; Escherichia coli; Mutation; Plasmids; Transduction, Genetic

|- class="tableEdit_footer"
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|}


==Main Points of the Paper ==
{{LitSignificance}}

== Materials and Methods Used ==
{{LitMaterials}}

==Phenotype Annotations==
{{AnnotationTableHelp}}
<protect>

{| id="Y4f99846ddc28e" class=" tableEdit Phenotype_Table_2"
|-
!|Phenotype of!!Taxon Information!!Genotype Information (if known)!!Condition Information!!OMP ID!!OMP Term Name!!ECO ID!!ECO Term Name!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.3046.Y4f99846ddc28e&page=3046&pagename={{FULLPAGENAMEE}}&type=0&template=Phenotype_Table_2 edit table] || || || || || || || || ||
|}
</protect>

==Notes==

==References==
{{RefHelp}}
<references/>

[[Category:Publication]]

PMID:783128

2012-04-26T17:22:53Z

165.91.108.7: New PMID: Page!

PMID:2176633

2012-04-20T18:13:25Z

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{| id="F4f91a744dd954" class=" tableEdit PMID_info_table"

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!align=left |Citation
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'''Trun, NJ and Gottesman, S''' (1990) On the bacterial cell cycle: Escherichia coli mutants with altered ploidy.''Genes Dev.'' '''4''':2036-47
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!align=left |Abstract
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We describe a scheme for isolation of new classes of mutants in the cell cycle of Escherichia coli. The mutants were selected as resistant to camphor vapors, which results in increased ploidy, and were subsequently screened for an increase in cell density and an increase in the gene dosage of the lac operon. Our mutations are located at four different places in the chromosome; we have named these loci mbr (moth ball resistant). mbrA maps to 68 min on the E. coli chromosome, mbrB to 88.5 min, mbrC to 89.5 min, and mbrD to 90 min. mbrD mutations may be alleles of rpoB (a subunit of RNA polymerase). In addition to the selected or screened phenotypes, most of the mutants fail to grow on rich media or at high temperatures. We have examined the nine mutants under nonpermissive conditions, using several techniques to determine the cause of death. We have also coupled our mutations with lesions in dnaA, which is required for cell-cycle-specific DNA replication, and rnh (the gene for RNase H), which is required for specificity in the DNA initiation reaction, and determined the effects of the double and triple mutants under permissive and nonpermissive conditions. These tests have shown that bacteria mutated at mbrA do not tolerate a null mutation in rnh, indicating that they are dependent on DNA replication initiating at oriC. In contrast, mutations at mbrB, mbrC, and mbrD exhibit their phenotypes independent of oriC initiation of DNA replication, suggesting that the mutations affect factors that influence the DNA/cell ratio regardless of the origin of DNA replication. Based on our results, the mbr mutations appear to have defects in cell-cycle timing and/or defects in chromosomal partitioning.
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!align=left |Links
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2176633 PubMed]

|-
!align=left |Keywords
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Camphor; Cell Cycle; Chromosome Mapping; Chromosomes, Bacterial; DNA Replication; DNA, Bacterial; DNA-Directed RNA Polymerases; Drug Resistance, Microbial; Endoribonucleases; Escherichia coli; Mutation; Phenotype; Ploidies; Ribonuclease H

|- class="tableEdit_footer"
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|}


==Main Points of the Paper ==
{{LitSignificance}}

== Materials and Methods Used ==
{{LitMaterials}}

==Phenotype Annotations==
{{AnnotationTableHelp}}
<protect>

{| id="H4f91a744dff4e" class=" tableEdit Phenotype_Table_2"
|-
!|Phenotype of!!Taxon Information!!Genotype Information (if known)!!Condition Information!!OMP ID!!OMP Term Name!!ECO ID!!ECO Term Name!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.2990.H4f91a744dff4e&page=2990&pagename={{FULLPAGENAMEE}}&type=0&template=Phenotype_Table_2 edit table] || || || || || || || || ||
|}
</protect>

==Notes==

==References==
{{RefHelp}}
<references/>

[[Category:Publication]]

PMID:2176633

2012-04-20T18:13:24Z

165.91.108.7: New PMID: Page!

PMID:1925019

2012-04-20T18:12:33Z

165.91.108.7: Fill PMID: Page!

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{| id="R4f91a710dceeb" class=" tableEdit PMID_info_table"

|-
!align=left |Citation
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'''Trun, NJ and Gottesman, S''' Characterization of Escherichia coli mutants with altered ploidy.''Res. Microbiol.'' '''142''':195-200
|-
!align=left |Abstract
||
We describe the isolation and characterization of new mutants in the cell cycle of Escherichia coli. The mutants were selected as gain of function mutants that are able to maintain more than the normal number of chromosomes. Our increased ploidy mutants were isolated as resistant to camphor vapours, which selects for cells with more chromosomes than normal. The mutants (called mbr for moth-ball-resistant) map to four chromosomal locations: mbrA at 68 min; mbrB at 88.5 min; mbrC at 89.5 min; and mbrD at 90 min. To investigate the nature of these cell cycle mutants, we have coupled them with defects in recA, to test for induction of the SOS response, and dam, to determine if methylation is required for mbr function. Based on the results of these and other tests, we have made a preliminary placement of the mbr mutants within the context of the cell cycle. mbrA mutations appear to be defective in the coupling of the DNA replication cycle to the cell division cycle, and as such, may define a new link between the two processes. mbrB does not seem to be able to coordinate the cell cycle and the growth rate of the cell. mbrC appears to be defective in partitioning of chromosomes. mbrD, which may be allelic to rpoB (a subunit of RNA polymerase), appears to be defective in either chromosomal partitioning or the later stages of DNA replication.
|-
!align=left |Links
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1925019 PubMed]

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!align=left |Keywords
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Camphor; Cell Cycle; Cell Division; DNA Replication; Drug Resistance, Microbial; Escherichia coli; Genes, Bacterial; Genes, Dominant; Mutation; Ploidies; Replicon

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.2989.R4f91a710dceeb&page=2989&pagename={{FULLPAGENAMEE}}&type=1&template=PMID_info_table edit table] ||
|}


==Main Points of the Paper ==
{{LitSignificance}}

== Materials and Methods Used ==
{{LitMaterials}}

==Phenotype Annotations==
{{AnnotationTableHelp}}
<protect>

{| id="P4f91a710e234e" class=" tableEdit Phenotype_Table_2"
|-
!|Phenotype of!!Taxon Information!!Genotype Information (if known)!!Condition Information!!OMP ID!!OMP Term Name!!ECO ID!!ECO Term Name!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.2989.P4f91a710e234e&page=2989&pagename={{FULLPAGENAMEE}}&type=0&template=Phenotype_Table_2 edit table] || || || || || || || || ||
|}
</protect>

==Notes==

==References==
{{RefHelp}}
<references/>

[[Category:Publication]]

PMID:1925019

2012-04-20T18:12:32Z

165.91.108.7: New PMID: Page!

PMID:2477554

2012-04-02T19:43:00Z

165.91.108.7: Fill PMID: Page!

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{| id="J4f7a01429a654" class=" tableEdit PMID_info_table"

|-
!align=left |Citation
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'''Allen, PN and Noller, HF''' (1989) Mutations in ribosomal proteins S4 and S12 influence the higher order structure of 16 S ribosomal RNA.''J. Mol. Biol.'' '''208''':457-68
|-
!align=left |Abstract
||
We have studied the effects of protein mutations on the higher order structure of 16 S rRNA in Escherichia coli ribosomes, using a set of structure-sensitive chemical probes. Ten mutant strains were studied, which contained alterations in ribosomal proteins S4 and S12, including double mutants containing both altered S4 and S12. Two ribosomal ambiguity (ram) S4 mutant strains, four streptomycin resistant (SmR) S12 mutant strains, one streptomycin pseudodependent (SmP) S12 mutant strain, one streptomycin dependent (SmD) S12 mutant strain and two streptomycin independent (Sm1) double mutants (containing both-SmD and ram mutations) were probed and compared to an isogenic wild-type strain. In ribosomes from strains containing S4 ram mutations, nucleotides A8 and A26 become more reactive to dimethyl sulfate (DMS) at their N-1 positions. In ribosomes from strains bearing the SmD allele, A908, A909, A1413 and G1487 are significantly less reactive to chemical probes. These same effects are observed when the S4 and S12 mutations are present simultaneously in the double mutants. An interesting correlation is found between the reactivity of A908 and the miscoding potential of SmR, SmD, SmP and wild-type ribosomes; the reactivity of A908 increases as the translational error frequency of the ribosomes increases. In the case of ram ribosomes, the reactivity of A908 resembles that of wild-type, unless tRNA is bound, in which case it becomes hyper-reactive. Similarly, streptomycin has little effect on A908 in wild-type ribosomes unless tRNA is bound, in which case its reactivity increases to resemble that of ram ribosomes with bound tRNA. Finally, interaction of streptomycin with SmP and SmD ribosomes causes the reactivity of A908 to increase to near-wild-type levels. A simple model is proposed, in which the reactivity of A908 reflects the position of an equilibrium between two conformational states of the 30 S subunit, one of which is DMS-reactive, and the other DMS-unreactive. In this model, the balance between these two states would be influenced by proteins S4 and S12. Mutations in S12 generally cause a shift toward the unreactive conformer, and in the case of SmD and SmP ribosomes, this shift can be suppressed phenotypically by streptomycin, ram mutations in protein S4 cause a shift toward the reactive conformer, but only when tRNA is bound. This suggests that the opposing effects of these two classes of mutations influence the proof-reading process by somewhat different mechanisms.
|-
!align=left |Links
||
[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2477554 PubMed]

|-
!align=left |Keywords
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Autoradiography; Bacterial Proteins; Escherichia coli; Models, Genetic; Mutation; RNA Probes; RNA, Bacterial; RNA, Ribosomal; RNA, Ribosomal, 16S; RNA, Transfer; Ribosomal Proteins; Streptomycin

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.2903.J4f7a01429a654&page=2903&pagename={{FULLPAGENAMEE}}&type=1&template=PMID_info_table edit table] ||
|}


==Main Points of the Paper ==
{{LitSignificance}}

== Materials and Methods Used ==
{{LitMaterials}}

==Phenotype Annotations==
{{AnnotationTableHelp}}
<protect>

{| id="G4f7a0144ac571" class=" tableEdit Phenotype_Table_2"
|-
!|Phenotype of!!Taxon Information!!Genotype Information (if known)!!Condition Information!!OMP ID!!OMP Term Name!!ECO ID!!ECO Term Name!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.2903.G4f7a0144ac571&page=2903&pagename={{FULLPAGENAMEE}}&type=0&template=Phenotype_Table_2 edit table] || || || || || || || || ||
|}
</protect>

==Notes==

==References==
{{RefHelp}}
<references/>

[[Category:Publication]]

PMID:2477554

2012-04-02T19:42:57Z

165.91.108.7: New PMID: Page!