Disease relevance of minC

• Central role for the Escherichia coli minC gene product in two different cell division-inhibition systems [1].
• The activity of the promoter regions of the cell division genes ftsZ, ftsE, minC, minD and minE from Neisseria gonorrhoeae (Ng) was studied under different environmental conditions using lacZ translational fusions [2].

High impact information on minC

• MinE accomplishes this by imparting topological specificity to a division inhibitor coded by the minC and minD genes [3].
• The two minC-dependent division-inhibition systems could be functionally distinguished by their different responses to the minE gene product [1].
• In this paper we show that one of the components of this division-inhibition system, the minC gene product, is also an essential component of another division-inhibition system, which is induced by derepression of the dicB gene and leads to inhibition of septation at all potential division sites [1].
• The average cellular positions of the ftsQAZ region (2 min) and the minB region (26.5 min) during the cell cycle was determined by fluorescent in situ hybridization using the position of oriC as a reference point [4].
• Separated minB foci appeared towards the end of DNA replication [4].

Biological context of minC

• The B. subtilis min genes were part of an operon transcribed from a major promoter more than 2.5 kb upstream from minC [5].
• Insertional inactivation of either minC or minD or the presence of the divIVB region on plasmids produces a severe minicell phenotype in wild-type cells [6].
• We report the cloning of the wild-type allele of divIVB1 and show that the mutation lies within a stretch of DNA containing two open reading frames whose predicted products are in part homologous to the products of the Escherichia coli minicell genes minC and minD [7].
• The second gene cluster contains two ORFs (minCD) homologous to minC and minD of E. coli but lacks a minE homolog [6].
• In Escherichia coli minB mutants, cell division can take place at the cell poles as well as non-polarly in the cell [8].

Other interactions of minC

• However, neither minC nor minD function was absolutely required for sporulation and, by implication, for asymmetric septum formation [5].

Analytical, diagnostic and therapeutic context of minC

• Autoradiography analysis as well as fluorescent staining of DNA showed that in addition to minicells, these strains and the original minB mutant also spontaneously produced anucleate rods of normal size and had an abnormal DNA distribution in filaments [9].
• DNA-less cell formation in dnaX(Ts), dnaX(Ts) sfiA, and the minB minicell-forming mutant is accompanied by a local increase in peptidoglycan synthesis at the constriction site [10].

References