Defects in CTP:PHOSPHORYLETHANOLAMINE CYTIDYLYLTRANSFERASE affect embryonic and postembryonic development in Arabidopsis.

A TILLING strategy (for targeting-induced local-scale lesions in genomes) was used in Arabidopsis thaliana to isolate mutants of a gene encoding CTP:PHOSPHORYLETHANOLAMINE CYTIDYLYLTRANSFERASE (PECT; EC 2.7.7.14), a rate-limiting enzyme in phosphatidylethanolamine biosynthesis. A null mutation, pect1-6, caused embryo abortion before the octant stage. However, reciprocal crosses revealed that pect1-6 caused no significant gametophytic defect. In pect1-4, PECT activity was decreased by 74%. Growth was generally normal in these mutants, despite delays in embryo maturation and reduced fertility. At low temperatures, however, homozygotic pect1-4 plants displayed dwarfism. PECT activity was decreased by 47% in heterozygotic pect1-6 plants and by 80% in pect1-4/pect1-6 F1 plants, which also displayed a small but significant decrease of phosphatidylethanolamine and a reciprocal increase in phosphatidylcholine. These lipid changes were fully reversed by wild-type PECT1 expression. pect1-4/pect1-6 F1 plants displayed severe dwarfism, tissue abnormalities, and low fertility, which was attributable in part to inhibition of anther, embryo, and ovule development, as was the reduced fertility of pect1-4 seedlings. PECT1 cDNA expression under the control of an inducible promoter partially rectified the mutant phenotypes observed in pect1-4/pect1-6 F1 seedlings, indicating that malfunctions in different tissues have a synergistic effect on the mutant phenotypes.