The gerC locus of Bacillus subtilis, required for menaquinone biosynthesis, is concerned only indirectly with spore germination.

Abstract

The gerC region of Bacillus subtilis comprises a tricistronic operon, encoding enzymes that catalyse the late stages of menaquinone biosynthesis. The gerC58 mutation is responsible for a severe growth defect; unsuppressed mutant cells grow as very short rods, which sometimes septate aberrantly. Cultures grow only to a low cell density, rapidly lose viability, and never sporulate. Unlinked suppressor mutations can restore near-normal growth. Several independent suppressed isolates were examined; all grew to normal cell length, but they showed, to varying extents, a residual defect in the placement of the cell division septum. The germination properties of the suppressed derivatives varied from normal to significantly slow in germination in all germinants; therefore, the combination of the gerC mutation and different suppressor alleles resulted in spores with very different germination properties. This suggests that any relationship between the gerC gene products and spore germination is indirect. The gerCC58 mutation maps in a gene encoding the catalytic subunit of the heptaprenyldiphosphate synthase, which is responsible for formation of the isoprenoid side chain of menaquinone-7, and it is proposed that the gerCA, gerCB and gerCC genes be renamed hepA, menG and hepB, respectively.