| First Author | Fullerton MD | Year | 2007 |
| Journal | Mol Cell Biol | Volume | 27 |
| Issue | 9 | Pages | 3327-36 |
| PubMed ID | 17325045 | Mgi Jnum | J:121387 |
| Mgi Id | MGI:3709941 | Doi | 10.1128/MCB.01527-06 |
| Citation | Fullerton MD, et al. (2007) Developmental and metabolic effects of disruption of the mouse CTP:phosphoethanolamine cytidylyltransferase gene (Pcyt2). Mol Cell Biol 27(9):3327-36 |
| abstractText | The CDP-ethanolamine pathway is responsible for the de novo biosynthesis of ethanolamine phospholipids, where CDP-ethanolamine is coupled with diacylglycerols to form phosphatidylethanolamine. We have disrupted the mouse gene encoding CTP:phosphoethanolamine cytidylyltransferase, Pcyt2, the main regulatory enzyme in this pathway. Intercrossings of Pcyt2(+/-) animals resulted in small litter sizes and unexpected Mendelian frequencies, with no null mice genotyped. The Pcyt2(-/-) embryos die after implantation, prior to embryonic day 8.5. Examination of mRNA expression, protein content, and enzyme activity in Pcyt2(+/-) animals revealed the anticipated 50% decrease due to the gene dosage effect but rather a 20 to 35% decrease. [(14)C]ethanolamine radiolabeling of hepatocytes, liver, heart, and brain corroborated Pcyt2 gene expression and activity data and showed a decreased rate of phosphatidylethanolamine biosynthesis in heterozygotes. Total phospholipid content was maintained in Pcyt2(+/-) tissues; however, this was not due to compensatory increases in the decarboxylation of phosphatidylserine. These results establish the necessity of Pcyt2 for murine development and demonstrate that a single Pcyt2 allele in heterozygotes can maintain phospholipid homeostasis. |
