Difference between revisions of "PMID:1938875"
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+ | {| id="V4f208314b9aa2" class=" tableEdit PMID_info_table" | ||
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+ | |- | ||
+ | !align=left |Citation | ||
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+ | '''Nurse, P, Zavitz, KH and Marians, KJ''' (1991) Inactivation of the Escherichia coli priA DNA replication protein induces the SOS response.''J. Bacteriol.'' '''173''':6686-93 | ||
+ | |- | ||
+ | !align=left |Abstract | ||
+ | || | ||
+ | Many of the proteins that operate at the replication fork in Escherichia coli have been defined genetically. These include some of the subunits of the DNA polymerase III holoenzyme, the DnaB replication fork helicase, and the DnaG primase. The multiprotein primosome (which includes the DnaB and DnaG proteins), defined biochemically on the basis of its requirement during bacteriophage phi X174 complementary-strand synthesis, could serve as the helicase-primase replication machine on the lagging-strand template. In order to determine if this is the case, we have begun an investigation of the phenotypes of mutants with mutations priA, priB, and priC, which encode the primosomal proteins factor Y (protein n'), n, and n", respectively. Inactivation of priA by insertional mutagenesis resulted in the induction of the SOS response, as evinced by induction of a resident lambda prophage, extreme filamentation, and derepression of an indicator operon in which beta-galactosidase production was controlled by the dinD1 promoter. In addition, the copy numbers of resident pBR322 plasmids were reduced four- to fivefold in these strains, and production of phi X174 phage was delayed considerably. These results are discussed in the context of existing models for SOS induction and possible roles for the PriA protein at the replication fork in vivo. | ||
+ | |- | ||
+ | !align=left |Links | ||
+ | || | ||
+ | [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1938875 PubMed] | ||
+ | |||
+ | |- | ||
+ | !align=left |Keywords | ||
+ | || | ||
+ | Bacterial Proteins; Blotting, Southern; DNA Replication; DNA, Bacterial; Escherichia coli; Genes, Bacterial; Mutagenesis, Insertional; Phenotype; SOS Response (Genetics) | ||
+ | |||
+ | |- class="tableEdit_footer" | ||
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+ | |} | ||
+ | <!--box uid=d41d8cd98f00b204e9800998ecf8427e.2835.V4f208314b9aa2--> | ||
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+ | ==Main Points of the Paper == | ||
+ | {{LitSignificance}} | ||
+ | |||
+ | == Materials and Methods Used == | ||
+ | {{LitMaterials}} | ||
+ | |||
+ | ==Phenotype Annotations== | ||
+ | {{AnnotationTableHelp}} | ||
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+ | * ** PLEASE DON'T EDIT THIS TABLE DIRECTLY. Use the edit table link under the table. ** | ||
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+ | {| border="2" cellpadding="4" cellspacing="0" style="margin: 1em 1em 1em 0; border: 1px #aaa solid; border-collapse: collapse;" id="F4f208314df2b0" class=" tableEdit Phenotype_Table_2" | ||
+ | |- align='left' bgcolor='#CCCCFF' | ||
+ | !|Phenotype of!!Taxon Information!!Genotype Information (if known)!!Condition Information!!OMP ID!!OMP Term Name!!ECO ID!!ECO Term Name!!Notes!!Status | ||
+ | |- | ||
+ | | | ||
+ | a mutation or genetic difference within a strain | ||
+ | | | ||
+ | *Taxon: Escherichia coli | ||
+ | *Strain: K-12 | ||
+ | *Substrain: | ||
+ | *NCBI Taxon ID: [http://www.ncbi.nlm.nih.gov/taxonomy?term=83333 83333] | ||
+ | | | ||
+ | *Genotype of Reference Strain: ''priA'' | ||
+ | *Genotype of Experimental Strain : ''priA::kan<sup>r</sup>'' | ||
+ | | | ||
+ | *Reference Condition: | ||
+ | | | ||
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+ | | | ||
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+ | | | ||
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+ | Inactivation of priA showed huge multinucleoid cell filaments, Fig 4B. | ||
+ | | | ||
+ | |||
+ | |- | ||
+ | | | ||
+ | a mutation or genetic difference within a strain | ||
+ | | | ||
+ | *Taxon: Escherichia coli | ||
+ | *Strain: K-12 | ||
+ | *Substrain: | ||
+ | *NCBI Taxon ID: [http://www.ncbi.nlm.nih.gov/taxonomy?term=83333 83333] | ||
+ | | | ||
+ | *Genotype of Reference Strain: ''priA'' | ||
+ | *Genotype of Experimental Strain : ''priA::kan<sup>r</sup>'' | ||
+ | | | ||
+ | *Reference Condition: | ||
+ | | | ||
+ | |||
+ | | | ||
+ | |||
+ | | | ||
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+ | | | ||
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+ | Inactivation causes slow growth rate, fig 3. | ||
+ | | | ||
+ | |||
+ | |- | ||
+ | | | ||
+ | a mutation or genetic difference within a strain | ||
+ | | | ||
+ | *Taxon: Escherichia coli | ||
+ | *Strain: K-12 | ||
+ | *Substrain: PN101 | ||
+ | *NCBI Taxon ID: [http://www.ncbi.nlm.nih.gov/taxonomy?term=83333 83333] | ||
+ | | | ||
+ | *Genotype of Reference Strain: ''priA+'' | ||
+ | *Genotype of Experimental Strain : ''priA2::kan'' | ||
+ | | | ||
+ | *Reference Condition: | ||
+ | | | ||
+ | |||
+ | | | ||
+ | |||
+ | | | ||
+ | ECO:0000003 | ||
+ | | | ||
+ | reconstitution assay evidence | ||
+ | | | ||
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+ | | | ||
+ | |||
+ | |||
+ | |- class="tableEdit_footer" | ||
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+ | |} | ||
+ | <noinclude> | ||
+ | |||
+ | </noinclude> | ||
+ | <!--box uid=d41d8cd98f00b204e9800998ecf8427e.2835.F4f208314df2b0--></protect> | ||
+ | |||
+ | ==Notes== | ||
+ | |||
+ | ==References== | ||
+ | {{RefHelp}} | ||
+ | <references/> | ||
+ | |||
+ | |||
+ | [[Category:Publication]] |
Latest revision as of 15:43, 3 June 2015
Citation |
Nurse, P, Zavitz, KH and Marians, KJ (1991) Inactivation of the Escherichia coli priA DNA replication protein induces the SOS response.J. Bacteriol. 173:6686-93 |
---|---|
Abstract |
Many of the proteins that operate at the replication fork in Escherichia coli have been defined genetically. These include some of the subunits of the DNA polymerase III holoenzyme, the DnaB replication fork helicase, and the DnaG primase. The multiprotein primosome (which includes the DnaB and DnaG proteins), defined biochemically on the basis of its requirement during bacteriophage phi X174 complementary-strand synthesis, could serve as the helicase-primase replication machine on the lagging-strand template. In order to determine if this is the case, we have begun an investigation of the phenotypes of mutants with mutations priA, priB, and priC, which encode the primosomal proteins factor Y (protein n'), n, and n", respectively. Inactivation of priA by insertional mutagenesis resulted in the induction of the SOS response, as evinced by induction of a resident lambda prophage, extreme filamentation, and derepression of an indicator operon in which beta-galactosidase production was controlled by the dinD1 promoter. In addition, the copy numbers of resident pBR322 plasmids were reduced four- to fivefold in these strains, and production of phi X174 phage was delayed considerably. These results are discussed in the context of existing models for SOS induction and possible roles for the PriA protein at the replication fork in vivo. |
Links | |
Keywords |
Bacterial Proteins; Blotting, Southern; DNA Replication; DNA, Bacterial; Escherichia coli; Genes, Bacterial; Mutagenesis, Insertional; Phenotype; SOS Response (Genetics) |
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Main Points of the Paper
Please summarize the main points of the paper.
Materials and Methods Used
Please list the materials and methods used in this paper (strains, plasmids, antibodies, etc).
Phenotype Annotations
See Help:AnnotationTable for details on how to edit this table.
Phenotype of | Taxon Information | Genotype Information (if known) | Condition Information | OMP ID | OMP Term Name | ECO ID | ECO Term Name | Notes | Status |
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a mutation or genetic difference within a strain |
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Inactivation of priA showed huge multinucleoid cell filaments, Fig 4B. |
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a mutation or genetic difference within a strain |
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Inactivation causes slow growth rate, fig 3. |
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a mutation or genetic difference within a strain |
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ECO:0000003 |
reconstitution assay evidence |
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Notes
References
See Help:References for how to manage references in OMPwiki.