Human lipoprotein lipase last exon is not translated, in contrast to lower vertebrates

被引:25
作者
Arnault, F
Etienne, J
Noe, L
Raisonnier, A
Brault, D
Harney, JW
Berry, MJ
Tse, C
FromentalRamain, C
Hamelin, J
Galibert, F
机构
[1] FAC MED ST ANTOINE TENON, LAB BIOCHIM & BIOL MOL, F-75970 PARIS 20, FRANCE
[2] CHU PITIE SALPETRIERE, F-75634 PARIS 13, FRANCE
[3] HARVARD UNIV, BRIGHAM & WOMENS HOSP, SCH MED, DIV THYROID, BOSTON, MA 02115 USA
[4] ULP, COLL FRANCE,INSERM,CNRS, INST GENET & BIOL MOL & CELLULAIRE, F-67404 ILLKIRCH GRAFFENSTADEN, FRANCE
[5] FAC MED, CNRS, UPR 41, F-35043 RENNES, FRANCE
关键词
fish intron; zebrafish LPL; rainbow trout LPL; lipoprotein lipase (LPL); LPL intron 9; LPL exon 10; 3'UTR; selenoprotein; deiodinase; SECIS elements;
D O I
10.1007/BF02337355
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We have sequenced the first fish (zebrafish, Brachydanio rerio) lipoprotein lipase (LPL) cDNA clone. Similarities were found in mammalian LPL cDNA, but the codon spanning the last two exons (which is thus split by the last intron) is AGA (Arg) as opposed to TGA in mammals. Exon 10 is thus partially translated. These results were confirmed with rainbow trout (Oncorhynchus mykiss). We also investigated whether mammal TGA coded for selenocystein (SeCys), the 21st amino acid, but found that this was not the case: TGA does not encode SeCys but is a stop codon. It thus appears that the sense codon AGA (fish) has been transformed into a stop codon TGA (human) during the course of evolution. It remains to be determined if the ''loss'' of the C-terminal end of mammalian LPL protein has conferred an advantage in terms of LPL activity or, on the contrary, a disadvantage (e.g., susceptibility to diabetes or atherosclerosis).
引用
收藏
页码:109 / 115
页数:7
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