Role of vitamin K2 in the organization and function of Staphyloccus aureus membranes

Abstract

A mutant of Staphylococcus aureus auxotrophic for menadione (a vitamin K2 precursor) was used to study the effects of menadione deprivation on the structure and function of the cell membrane. The phospholipid composition and metabolism was essentially unaltered by menadione deprivation. Removal of this precursor caused cellular levels of the cytochromes, protoheme, vitamin K2, and several membrane bound flavoprotein dehydrogenase activities to decrease as a function of growth dilution. The cytochromes were enzymatically reducible and maintained in the same proportions as menadione supplemented cells. Oxidative phosphorylation, however, was reduced more than 10 fold and membrane vesicles obtained from menadione deprived cells were unable to couple glycine transport to L lactate oxidation. Succinic dehydrogenase and adenosine 5' triphosphate hydrolysis appeared unaffected by menadione deprivation. These data suggest that menadione deprivation in the mutant stops the synthesis of vitamin K2 and other electron transport chain components and prosthetic groups. Although individual electron transport chain members remained fully functional during menadione deprivation, the overall efficiency of the chain, measured in terms of its function in electron transport, oxidative phosphorylation, and electron transport chain linked transport, dropped greatly. This suggests that the synthesis of vitamin K2 is modulated to the synthesis of other components of the electron transport system, and that their organization into a functional system requires a specific concentration of vitamin K2 with respect to total membrane lipid.