Disease relevance of minE

• The minCD locus of Bacillus subtilis lacks the minE determinant that provides topological specificity to cell division [1].
• Proper positioning of division sites in Escherichia coli requires balanced expression of minC, minD, and minE gene products [2].
• Two ylm homologues are also found in algal and plant genomes. cdv3 has low but significant similarity to divIVA, suggesting that minE and cdv3 both mediate division-site determination in cyanobacteria [3].
• In contrast, Gram-positive bacteria lack minE, and (Gram-negative) proteobacteria lack divIVA. ftn6, of unknown function, and the circadian input kinase, cikA, are specific to cyanobacteria [3].

High impact information on minE

• The most striking is the existence of two adjacent genes homologous to bacterial genes involved in cell division, minD and minE, which are arranged in the same order in Escherichia coli [4].
• The two minC-dependent division-inhibition systems could be functionally distinguished by their different responses to the minE gene product [5].
• These were found in strains in which chromosome replication or nucleoid segregation was disturbed, e.g. in minB mutants, intR1 strains, and in strains exhibiting stable DNA replication [6].
• The last two ORFs (minCD) are homologous to minC and minD of Escherichia coli but a minE homolog is lacking in B. subtilis [7].
• Disruption of the minE gene resulted in large, swollen and branched free-living cells, and in symbiosis a minE mutation resulted in a defect in nitrogen fixation with activity reduced by approximately 70 % compared to the wild-type [8].

References