Characteristics of cho2opi3 suppressor mutants in yeast generated in the presence of ethanolamine

Phosphatidylcholine (PC) is the most abundant phospholipid in human and yeast cells. It is crucial to maintain the homeostasis and membrane characteristics. In human cells it is a useful pharmacological target for the traitment of obesity and insuline resistence. In yeast, cells are able to produce PC by two different pathways: the CDP-DAG pathway and the Kennedy pathway. In the first one the phospholipid PE is converted in PC by a trimethylation reaction catalyzed by enzymes encoded by CHO2 and OPI3. In the Kennedy pathway, cells use exogenous choline and DAG to produce PC. Ethanolamine suppressors are new strains of Saccharomyces cereviseae with a double deletion of the genes CHO2 and OPI3. Four different ethanolamine suppressors were isolated, called N°1, 2, 3 and 4. The scientific interest in these strains arises from the ability of the cells to survive in the absence of PC, i.e. without exogenous choline but instead with ethanolamine addition into the growth media. The main phospholipid in the ethanolamine suppressors is phosphatidylethanolamine (PE), the metabolic precursor of PC. This phospholipid is produced by the cell by the Kennedy pathway using exogenous ethanolamine. PE presents structural difference with PC like a smaller head-group, the ability to form H-bonds, and a conical shape, therefore it is considered a non-bilayer lipid. To maintain the membrane homeostasis, ethanolamine suppressors modified the phospholipids' profile. The cells modified the percentage abundance of each different phospholipid and remodeled the acyl chains to maintain the membrane negative curvature. Consequently, the neutral lipids' profile was also modified. All the modification are connected via regulation at the level of gene expression. In the research reported, a characterisation study was conducted on the four ethanolamine suppressors focusing on the phospholipid and neutral lipid profile, acyl chain modifications, growth ability in different media and INO1 regulation.