Vegetative cell division in Bacillus subtilis takes place precisely at the middle of the cell to ensure that two viable daughter cells are formed. The first event in cell division is the positioning of the FtsZ Z-ring at the correct site. This is controlled by the coordinated action of both negative and positive regulators. The existence of positive regulators has been inferred, but none have presently been identified in B. subtilis. Noc and the Min system belong to negative regulators; Noc prevents division from occurring over the chromosomes, and the Min system inhibits cell division at the poles. Here we report that the morphogenic protein, RodZ, an essential cell shape determinant, is also required for proper septum positioning during vegetative growth. In rodZ mutant cells, the vegetative septum is positioned off center, giving rise to small, round, DNA-containing cells. Searching for the molecular mechanism giving rise to this phenotype led us to discover that RodZ directly interacts with MinJ. We hypothesize that RodZ may aid the Min system in preventing non-medial vegetative division.

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In yeasts, the PDR16 gene encodes a phosphatidylinositol transfer protein which belongs to the Sec14 homologue (SFH) family and localizes to lipid droplets, microsomes and at the cell periphery. The loss of its function alters the lipid droplet metabolism and plasma membrane properties, and renders yeast cells more sensitive to azole antimycotics. In this study, the entire chromosomal CgPDR16 ORF was replaced by the ScURA3 gene both in azole sensitive and azole resistant strains of Candida glabrata bearing a gain-of-function mutation in the CgPDR1 gene, and their responses to different stresses were assessed. The CgPDR16 deletion was found to sensitize the mutant strains to azole antifungals without changes in their osmo- and halotolerance. Fluconazole treated pdr16Δ mutant strains displayed a reduced expression of several genes involved in azole tolerance. The gain-of-function CgPDR1 allele as well as the cycloheximide and hydrogen peroxide treatments of cells enhanced the expression of the CgPDR16 gene. The results indicate that CgPDR16 belongs to genes whose expression is induced by chemical and oxidative stresses. The loss of its function can attenuate the expression of drug efflux pump encoding genes that might also contribute to the decreased azole tolerance in pdr16Δ mutant cells.