Phospholipid Variations in Mutant Strains of Neurospora Crassa.

The present studies were undertaken to determine the extent to which the phospholipid composition of Neurosporn crama can be altered by mutations studied in conjunction with controlled supplementation. Previous work in this laboratory has shown that a mutation involving an enzyme concerned with lecithin synthesis can result in a lecithin-deficient strain (1, 2). The methylation of phosphatidylethanolamine appears to be the major metabolic source of lecithin when N. crassa is grown on minimal medium (3). Two mutant strains, 34486 and 47904, are known with aberrations concerning one or more of the three methylations involved in this metabolic sequence leading to lecithin synthesis (4, 5). These lecithin-deficient organisms show a growth response to exogenous supplements of either choline or dimethylethanolamine, and strain 34486 also utilizes monomethylethanolamine for growth. These growth response experiments indicate that N. crassa incorporates the three methylated ethanolamines into phospholipids by pathways analogous to those known in other species, involving the cytidine diphosphate derivatives of these ethanolamines as obligatory intermediates (68). Since N. crassa has two independent metabolic pathways leading to lecithin formation, its phospholipid composition may be altered by controlling the relative contribution of these two synthetic systems. Two mutations were used to alter the substrate turnover by the phospholipid-methylating enzymes, and the contribution of the alternate routes, presumably the cytidine nucleotide pathways, to the synthesis of phospholipids was influenced by supplementation of cultures with methylated ethanolamines.