Fig. 7
Metabolic strategy in evolved strains lacking the aas-lplT operon. Proposed phosphatidylethanolamine (PtdEtn) metabolism model in PB12 and PB13 strains where the deletion of aas-lplT operon is responsible of the lack of the 2-acyl-GPE cycle that in turn was apparently replaced with the utilization of the degradation pathway. In these evolved strains two additional mutations were detected: in the glpT and dhaM genes. At least the glpT mutation could be playing a role in these strains for PtdEtn utilization and faster growth on glucose. The abbreviations are as follows: phosphatidylethanolamine (PtdEtn), 2-acyl-glycerophosphatidylethanolamine (2-acyl-GPE), fatty acid (FA), Lipoprotein (Lpp), acylated lipoprotein (Acyl-Lpp), Apolipoprotein N-acyltransferase (Lnt), phospholipase A type 2 (PLA2), phosphatidylethanolamine transporter in the 2-acyl-GPE cycle (MsbA), lysophospholipid transporter (LplT), 1-acylglycerol-3-phosphate O-acyltransferase (PlsC), 2-acylglycerophosphoethanolamine acyltransferase/acyl-ACP synthetase (Aas), acyl-ACP synthetase activity (ACP), 2-acylglycerophosphoethanolamine acyltransferase activity (ACS), glycerophosphoryl diester phosphodiesterase (GlpQ), fatty acyl-CoA synthetase (FadD), glycerol-3-phosphate:phosphate antiporter (GlpT)