These Pltp knock-out mice exhibit decreases in plasma HDL phospholipid, cholesteryl ester, free cholesterol, and apoAI.
Xian-cheng Jiang, Columbia University
Mice that are homozygous null for the Pltp gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Pltp mRNA is detected in the tissues that normally express Pltp (lung and liver). No plasma Pltp activity is detected. Marked decreases in plasma HDL phospholipid (66%), cholesteryl ester (69%), free cholesterol (70%) and apoAI are observed. When mice are maintained on a high fat/high cholesterol diet, similar reductions are observed, as are increases in VLDL and LDL phospholipid, free cholesterol and cholesteryl ester. This mutant strain offers a model useful in studies related to cholesterol metabolism and atherosclerosis.
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt a region of the Pltp gene encoding intron 1, exon 2 and a portion of intron 2. The construct was electroporated into 129P2/OlaHsd-derived E14 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric male animals were backcrossed to C57BL/6 females.
|Allele Name||targeted mutation 1, Xian-cheng Jiang|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Pltp, phospholipid transfer protein|
|Gene Synonym(s)||BPIFE; Bpife; HDLCQ9; OD107|
|Strain of Origin||Not Specified|
|General Note||Phenotypic Similarity to Human Syndrome: Dry Eye Syndrome (J:171592).|
|Molecular Note||A neomycin selection cassette replaced a genomic fragment containing exon 2, which encodes the initiation codon, the signal peptide and the first 16 amino acids of the mature protein. Northern blot and RNase protection analysis on RNA derived from lung of homozygous mice demonstrated that no detectable transcript was produced from this allele. Activity assays on plasma of homozygous mice confirmed that no functional protein was expressed from this allele.|
|Mutations Made By|| |
Xian-cheng Jiang, Columbia University
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