Difference between revisions of "PMID:15916962"

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==Main Points of the Paper ==
 
==Main Points of the Paper ==
{{LitSignificance}}
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*''slmA'' is synthetically lethal with ''minB''
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*Nucleoid cutting results in ''slmA'' mutants, indicating SlmA has a role in septal ring positioning
  
 
== Materials and Methods Used ==
 
== Materials and Methods Used ==
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!|Species!!Taxon ID!!Strain!!Gene (if known)!!OMP!!Phenotype!!Details!!Evidence!!Notes
 
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''Escherichia coli''
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TB86
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slmA minB
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*filamentation
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*absent septation
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Morphology
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Microscopy
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Figure 1 and 2
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''Escherichia coli''
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TB105
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''slmA''
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nucleoid cutting/guillotining
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Morphology
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septal rings form and constrict over regions of DNA
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Microscopy
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Figure 3
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''Escherichia coli''
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TB86
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slmA minB
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no growth
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Morphology
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synthetic lethality
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Microscopy
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Figure 1
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''Escherichia coli''
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TB105
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''slmA''
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nucleoid free cells
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Morphology
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Microscopy
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Figure 3
  
 
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Latest revision as of 12:08, 22 June 2011

Citation

Bernhardt, TG and de Boer, PA (2005) SlmA, a nucleoid-associated, FtsZ binding protein required for blocking septal ring assembly over Chromosomes in E. coli.Mol. Cell 18:555-64

Abstract

Cell division in Escherichia coli begins with assembly of the tubulin-like FtsZ protein into a ring structure just underneath the cell membrane. Spatial control over Z ring assembly is achieved by two partially redundant negative regulatory systems, the Min system and nucleoid occlusion (NO), which cooperate to position the division site at midcell. In contrast to the well-studied Min system, almost nothing is known about how Z ring assembly is blocked in the vicinity of nucleoids to effect NO. Reasoning that Min function might become essential in cells impaired for NO, we screened for mutations synthetically lethal with a defective Min system (slm mutants). By using this approach, we identified SlmA (Ttk) as the first NO factor in E. coli. Our combined genetic, cytological, and biochemical results suggest that SlmA is a DNA-associated division inhibitor that is directly involved in preventing Z ring assembly on portions of the membrane surrounding the nucleoid.

Links

PubMed Online version:10.1016/j.molcel.2005.04.012

Keywords

Carrier Proteins; Cell Division; Cell Membrane; Chromosomes, Bacterial; DNA Mutational Analysis; Escherichia coli; Escherichia coli Proteins; Recombinant Fusion Proteins

Main Points of the Paper

  • slmA is synthetically lethal with minB
  • Nucleoid cutting results in slmA mutants, indicating SlmA has a role in septal ring positioning

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.
<protect>

Species Taxon ID Strain Gene (if known) OMP Phenotype Details Evidence Notes

Escherichia coli

TB86

slmA minB

  • filamentation
  • absent septation

Morphology

Microscopy

Figure 1 and 2

Escherichia coli

TB105

slmA

nucleoid cutting/guillotining

Morphology

septal rings form and constrict over regions of DNA

Microscopy

Figure 3

Escherichia coli

TB86

slmA minB

no growth

Morphology

synthetic lethality

Microscopy

Figure 1

Escherichia coli

TB105

slmA

nucleoid free cells

Morphology

Microscopy

Figure 3

</protect>

Notes

References

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