Septation deficiency and phosphilipid perturbation in Escherichia coli genetically constitutive for the beta oxidation pathway.
Mutants of Escherichia coli defective in the regulation of the fatty acids beta oxidation pathway show an ultrastructural deficiency in septum formation at high growth rate. Several independent pairs of parent and mutant strains have been analyzed biochemically. Each parent strain displays a well-defined pattern of cellular phospholipids, which varies with the growth conditions. High ratios of phosphatidylglycerol to cardiolipin characterize fast-growth conditions. None of the mutant strains, although they grow in mass nearly as rapidly as their respective parents, can reach these high ratios. The beta oxidation pathway regulatory mutation leads to an increased turnover of the glycerol moieties of these phospholipids in the inner as well as in the outer cell membrane.
D000085:Acetates / Q000378:metabolism; D002308:Cardiolipins / Q000378:metabolism; D004926:Escherichia coli / Q000254:growth & development* / Q000378:metabolism / Q000648:ultrastructure; D005227:Fatty Acids / Q000378:metabolism*; D005796:Genes; D005990:Glycerol / Q000378:metabolism; D005994:Glycerophosphates / Q000378:metabolism; D009154:Mutation; D010715:Phosphatidylglycerols / Q000378:metabolism; D010743:Phospholipids / Q000378:metabolism*
D000085:Acetates; D002308:Cardiolipins; D005227:Fatty Acids; D005994:Glycerophosphates; D010715:Phosphatidylglycerols; D010743:Phospholipids; D005990:Glycerol