parC:Gene

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Nomenclature Location(s) and DNA Sequence Sequence Features Alleles and Phenotypes Genetic Interactions Genetic Resources Accessions Links References Suggestions

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Nomenclature

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Standard name

parC

Mnemonic

partitioning of the nucleoid Partition

Synonyms

ECK3010, b3019, JW2987[1], JW2987

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Notes

Location(s) and DNA Sequence

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Strain Map location Genome coordinates Genome browsers Sequence links

MG1655

68.15 minutes 

MG1655: 3163995..3161737
<gbrowseImage> name=NC_000913:3161737..3163995 source=MG1655 preset=GeneLocation </gbrowseImage>

REL606

NC_012967: 3100145..3097887
<gbrowseImage> name=NC_012967:3097887..3100145 source=REL606 preset=GeneLocation </gbrowseImage>

BW2952

NC_012759: 3048885..3051143
<gbrowseImage> name=NC_012759:3048885..3051143 source=BW2952 preset=GeneLocation </gbrowseImage>

W3110

 

W3110: 3164629..3162371
<gbrowseImage> name=NC_007779:3162371..3164629 source=W3110 preset=GeneLocation </gbrowseImage>

DH10B

DH10B: 3261740..3259482
<gbrowseImage> name=NC_010473:3259482..3261740 source=DH10B preset=GeneLocation </gbrowseImage>

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Notes

Sequence Features

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Feature Type Strain Genomic Location Evidence Reference Notes
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Notes

Alleles and Phenotypes

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Allele Nt change(s) AA change(s) Phenotype: Type Phenotype: Description Reference Availability Comments

parC1215

G2199A

G703D

Growth Phenotype

  • ts @ 42
  • Chromosome partitioning phenotype
  • Filamentation

PMID:2170028[2], PMID:2842295[3]

actual nucleotide mapping was referenced in [2]

parC10

Y120H

DNA nicking independent of ATP hydrolysis

PMID:9077455[4]

parCL80

S80L

Resistant to

Quinolone resistance

PMID:8524852[5]

The mutation conferred increased resistance toward quinolones, specifically norfloxcin. See figure 3. chEBI:23765

parCL80 gyrAr

parC S80L gyrA S83L

Resistant to

quinolone resistance

PMID:8524852[5]

The double mutation conferred a 6 fold increase of quinolone resistance compared to the mutation with only the gyrAR mutation. See figure 4 for experimental results. chEBI:23765

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Notes

  • The partitioning defect comes from the inability of these cells to partition the nucleoids into daughter cells. This results in filamentous cells with a cluster of nucleoid at the center and subsequent DNA-free cells.
  • The Keio collection[6] lists a deletion of parC, which is an essential gene. There is a duplication of the parC region.[7].
  • Suppressors of the parC1215 mutation when expressed at high-copy[8]:
    • topB
    • dnaN (β subunit of the DNA polymerase holoenzyme)
    • spcA (suppressor of parC A- will be renamed setB)


Genetic Interactions

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Interactor Interaction Allele Score(s) Reference(s) Accessions Notes
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Notes

Genetic Resources

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Resource Resource Type Source Notes/Reference

JW2987

Plasmid clone

Shigen

PMID:16769691[9]

Status:Clone OK

Primer 1:GCCAGCGATATGGCAGAGCGCCT

Primer 2:CCtTCTTCGCTATCACCGCTGCT

6H4

Kohara Phage

Genobase

PMID:3038334[10]

17B2

Kohara Phage

Genobase

PMID:3038334[10]

metC162::Tn10

Linked marker

CAG18475 = CGSC7435[11]

est. P1 cotransduction: 67% [12]

tolC210::Tn10

Linked marker

CAG12184 = CGSC7437[11]

est. P1 cotransduction: 56% [12]

plexBA-parEC

Plasmid Clone

  • IPTG-inducible Topo IV expression plasmid[13]

pLC4-14

Plasmid Clone

plasmid from the Clarke-Carbon collection

PMID:2842295[3]

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Notes

Accessions in Other Databases

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Database Accession Notes

EcoCyc

EcoCyc:EG10686

Escherichia coli str. K-12 substr. MG1655

EcoGene

EcoGene:EG10686

Escherichia coli str. K-12 substr. MG1655

RegulonDB

RegulonDB:ECK120000679

Escherichia coli str. K-12 substr. MG1655

NCBI (EcoliWiki Page)

GeneID:947499

Escherichia coli str. K-12 substr. MG1655

EchoBASE

EchoBASE:EB0680

Escherichia coli str. K-12 substr. MG1655

ASAP

ASAP:ABE-0009916

Escherichia coli str. K-12 substr. MG1655

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Notes

Links

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References

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  1. ↑ Riley, M. et al. (2006) Nucleic Acids Res 34:1-6 (corrected supplemental data from B. Wanner)
  2. ↑ 2.0 2.1 Kato, J et al. (1990) New topoisomerase essential for chromosome segregation in E. coli. Cell 63 393-404 PubMed
  3. ↑ 3.0 3.1 Kato, J et al. (1988) Gene organization in the region containing a new gene involved in chromosome partition in Escherichia coli. J. Bacteriol. 170 3967-77 PubMed
  4. ↑ Yokochi, T et al. (1996) DNA nicking by Escherichia coli topoisomerase IV with a substitution mutation from tyrosine to histidine at the active site. Genes Cells 1 1069-75 PubMed
  5. ↑ 5.0 5.1 Khodursky, AB et al. (1995) Topoisomerase IV is a target of quinolones in Escherichia coli. Proc. Natl. Acad. Sci. U.S.A. 92 11801-5 PubMed
  6. ↑ Baba, T et al. (2006) Construction of Escherichia coli K-12 in-frame, single-gene knockout mutants: the Keio collection. Mol. Syst. Biol. 2 2006.0008 PubMed
  7. ↑ Yamamoto, N et al. (2009) Update on the Keio collection of Escherichia coli single-gene deletion mutants. Mol. Syst. Biol. 5 335 PubMed
  8. ↑ Nurse, P et al. (2003) Topoisomerase III can serve as the cellular decatenase in Escherichia coli. J. Biol. Chem. 278 8653-60 PubMed
  9. ↑ Kitagawa, M et al. (2005) Complete set of ORF clones of Escherichia coli ASKA library (a complete set of E. coli K-12 ORF archive): unique resources for biological research. DNA Res. 12 291-9 PubMed
  10. ↑ 10.0 10.1 Kohara, Y et al. (1987) The physical map of the whole E. coli chromosome: application of a new strategy for rapid analysis and sorting of a large genomic library. Cell 50 495-508 PubMed
  11. ↑ 11.0 11.1 CGSC: The Coli Genetics Stock Center
  12. ↑ 12.0 12.1 The Tn10 insertion sites determined by Nichols et al. 1998 (PMID:9829956) were reannotated by alignment with E. coli K-12 genome sequence (GenBank accession NC_000913). P1 contransduction frequencies were calculated using the formula of Wu (PMID:5338813).
  13. ↑ Mossessova, E et al. (2000) Mutational analysis of Escherichia coli topoisomerase IV. I. Selection of dominant-negative parE alleles. J. Biol. Chem. 275 4099-103 PubMed

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