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The mouse phosphatidylethanolamine N ‐methyltransferase is regulated transcriptionally during hepatic perinatal development
Author(s) -
Cole Laura Kathleen,
Vance Dennis E
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a655-b
Subject(s) - microbiology and biotechnology , promoter , oligonucleotide , biology , transcription (linguistics) , gene , transcription factor , response element , chemistry , gene expression , biochemistry , linguistics , philosophy
Phosphatidylcholine (PC) is the predominant phospholipid in mammalian plasma lipoproteins and cellular membranes. A liver‐specific pathway for PC biosynthesis is catalyzed by phosphatidylethanolamine N ‐methyltransferase (PEMT). We have found using quantitative polymerase chain reaction that PEMT mRNA increases in the liver by 96‐fold during the perinatal period in mice. To determine regions within the Pemt promoter which are important for gene activation, we prepared sections of the Pemt promoter upstream of a luciferase reporter gene. Our preliminary data suggests that activation elements may exist between −471 and −371bp (relative to the transcriptional start site). This section of the Pemt promoter (−471 to −371bp) also binds nuclear factors from perinatal mouse liver nuclear extract as determined by electromobility shift assays (EMSA). We have identified, within this region, a conserved putative binding site (GC box) for a member of the Sp family of transcription factors. An oligonucleotide containing a GC box competed out the formation of a nuclear protein‐ Pemt promoter complex by EMSA. Furthermore, mutation of the GC box but not another region within the oligonucleotide eliminated this effect. These experiments suggest that a GC‐rich element may regulate the perinatal expression of the mouse Pemt gene. Supported by the Canadian Institutes for Health Research, the National Science and Engineering Research Council and the Alberta Heritage Foundation for Medical Research .