Disease relevance of dicA

• A mutation (dicA1) of a repressor gene located in the terminus region of the Escherichia coli chromosome has previously been shown to lead to temperature-dependent inhibition of division, and to be complemented by plasmids carrying either dicA or an adjacent gene dicC [1].

High impact information on dicA

• Five open reading frames (ORFs 1 to 5) preceeded by a promoter sensitive to dicA repression are found within a 1500 bp segment, and are organized into two clusters separated by a long untranslated region [2].
• A mutation in a gene dicA of Escherichia coli leads to temperature-sensitive cell division, by allowing expression of a nearby division inhibition gene dicB (1) [3].
• A second gene dicC transcribed divergently from dicA and coding for an 8.5 KD protein can also complement mutation dicA1 when provided on a multicopy plasmid [3].
• The defective gene in one of these mutants, dicA, was mapped at 34.9 min by linkage with manA and with three physically characterized Tn10 insertions [4].
• These results define the dicA-dicB locus as a new dispensable genetic cluster involved in the control of cell division [4].

Biological context of dicA

• In this study, operon fusions in the region coding for the division inhibition gene dicB have been used to show that temperature sensitivity does not result from high temperature inactivation of the dicA repressor [1].

References