Phosphatidylglycerol homeostasis in glycerol-phosphate auxotrophs of Staphylococcus aureus.

Journal Article


The balanced synthesis of membrane phospholipids, fatty acids and cell wall constituents is a vital facet of bacterial physiology, but there is little known about the biochemical control points that coordinate these activities in Gram-positive bacteria. In Escherichia coli, the glycerol-phosphate acyltransferase (PlsB) plays a key role in coordinating fatty acid and phospholipid synthesis, but pathogens like Staphylococcus aureus have a different acyltransferase (PlsY), and the headgroup of the major membrane phospholipid, phosphatidylglycerol (PtdGro), is used as a precursor for lipoteichoic acid synthesis.


The PlsY acyltransferase in S. aureus was switched off by depriving strain PDJ28 (ΔgpsA) of the required glycerol supplement. Removal of glycerol from the growth medium led to the rapid cessation of phospholipid synthesis. However, the continued utilization of the headgroup caused a reduction in PtdGro coupled with the accumulation of CDP-diacylglycerol and phosphatidic acid. PtdGro was further decreased by its stimulated conversion to cardiolipin. Although acyl-acyl carrier protein (ACP) and malonyl-CoA accumulated, fatty acid synthesis continued at a reduced level leading to the intracellular accumulation of unusually long-chain free fatty acids.


The cessation of new phospholipid synthesis led to an imbalance in membrane compositional homeostasis. PtdGro biosynthesis was not coupled to headgroup turnover leading to the accumulation of pathway intermediates. The synthesis of cardiolipin significantly increased revealing a stress response to liberate glycerol-phosphate for PtdGro synthesis. Acyl-ACP accumulation correlated with a decrease in fatty acid synthesis; however, the coupling was not tight leading to the accumulation of intracellular fatty acids.

Full Text

Duke Authors

Cited Authors

  • Parsons, JB; Yao, J; Jackson, P; Frank, M; Rock, CO

Published Date

  • November 16, 2013

Published In

Volume / Issue

  • 13 /

Start / End Page

  • 260 -

PubMed ID

  • 24238430

Pubmed Central ID

  • 24238430

Electronic International Standard Serial Number (EISSN)

  • 1471-2180

International Standard Serial Number (ISSN)

  • 1471-2180

Digital Object Identifier (DOI)

  • 10.1186/1471-2180-13-260


  • eng