Deletion Analysis of Gene minE Which Encodes the Topological Specificity Factor of Cell Division in Escherichia Coli

Mol Microbiol. 1995 Oct;18(2):321-9. doi: 10.1111/j.1365-2958.1995.mmi_18020321.x.


Division inhibition caused by the minCD gene products of Escherichia coli is suppressed specifically at mid-cell by MinE protein expressed at physiological levels. Excess MinE allows division to take place also at the poles, leading to a minicell-forming (Min-) phenotype. In order to investigate the basis of this topological specificity, we have analysed the ability of truncated derivatives of MinE to suppress either minCD-dependent division inhibition in a chromosomal delta(minB) background, or the division inhibition exerted by MinCD at the cell poles in a minB+ strain. Our results indicate that these two effects are not mediated by identical interactions of MinE protein. In addition, gel filtration and the yeast two-hybrid system indicated that MinE interacts with itself by means of its central segment. Taken together, our results favour a model in which wild-type MinE dimer molecules direct the division inhibitor molecules to the cell poles, thus preventing polar divisions and allowing non-polar sites to divide. This model explains how excess MinE, or an excess of certain MinE derivatives which prevent the accumulation of the division inhibitor at the poles, can confer a Min- phenotype in a minB+ strain.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Bacterial Proteins / genetics*
  • Cell Cycle Proteins
  • Cell Division / genetics*
  • Escherichia coli / genetics*
  • Escherichia coli Proteins*
  • Genes, Bacterial*
  • Molecular Sequence Data
  • Phenotype
  • Plasmids / genetics
  • Sequence Analysis
  • Sequence Deletion
  • Suppression, Genetic*


  • Bacterial Proteins
  • Cell Cycle Proteins
  • Escherichia coli Proteins
  • MinE protein, E coli