Role of SpoVG in asymmetric septation in Bacillus subtilis

Deletion of the citC gene, coding for isocitrate dehydrogenase, arrests spo rulation of Bacillus subtilis at stage I after bipolar localization of the cell division protein FtsZ but before formation of the asymmetric septum. A spontaneous extragenic suppressor mutation that overcame the stage I block was found to map within the spoVG gene. The suppressing mutation and other spoVG loss-of-function mutations enabled citC mutant cells to form asymmet ric septa and to activate the forespore-specific sigma factor sigma(F). How ever, little induction of mother cell-specific, sigma(E)-dependent sporulat ion genes was observed in a citC spoVG double mutant, indicating that there is an additional defect(s) in compartmentalized gene expression in the cit C mutant. These other defects could be partially overcome by reducing the s ynthesis of citrate, by buffering the medium, or by adding excess MnCl2. Ov erexpression of the spoVG gene in mild-type cells significantly delayed sig ma(F) activation. Increased expression and stability of SpoVG in citC mutan t cells may contribute to the citC mutant phenotype. Inactivation of the sp oVG gene caused a population of otherwise wild-type cells to produce a smal l number of minicells during growth and caused sporulating cells to complet e asymmetric septation more rapidly than normal. Unlike the case for inacti vation of the cell division inhibitor gene minD, many of these minicells co ntained DNA and appeared only when the primary sporulation signal transduct ion pathway, the Spo0A phosphorelay, was active. These results suggest that SpoVG interferes with or is a negative regulator of the pathway leading to asymmetric septation.