THE DIVIVA MINICELL LOCUS OF BACILLUS-SUBTILIS

The Bacillus subtilis divIVA1 mutation causes misplacement of the sept um during cell division, resulting in the formation of small, circular , anucleate minicells. This study reports the cloning and sequence ana lysis of 2.1 kb of the B. subtilis chromosome including the divIVA loc us. Three open reading frames were identified: orf whose function is u nknown; divIVA; and isoleucyl tRNA synthetase (ileS). We identified th e point mutation in the divIVA1 mutant allele. Inactivation of divIVA produces a minicell phenotype, whereas overproduction of DivIVA result s in a filamentation phenotype. Mutants with mutations at both of the minicell loci of B. subtilis, divIVA and divIVB, possess a minicell ph enotype identical to that of the DivIVB(-) mutant. The DivIVA(-) mutan ts, but not the DivIVB(-) mutants, show a decrease in sporulation effi ciency and a delay in the kinetics of endospore formation, The data su pport a model in which divIVA encodes the topological specificity subu nit of the minCD system. The model suggests that DivIVA acts as a pilo t protein, directing minCD to the polar septation sites. DivIVA also a ppears to be the interface between a sporulation component and MinCD, freeing up the polar septation sites for use during the asymmetric sep tation event of the sporulation process.