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J. Biol. Chem., Vol. 277, Issue 30, 26994-27005, July 26, 2002
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From the Muscle-type carnitine
palmitoyltransferase I (M-CPT I) is a key enzyme in the control of
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EBI Data Bank with accession number(s) AJ278284, AJ288906, and AJ288907.
Structural and Functional Genomics of the CPT1B Gene
for Muscle-type Carnitine Palmitoyltransferase I in Mammals*
§,
,,,,,, and
Department of Pediatrics, Groningen
University Institute for Drug Exploration, University of Groningen
and Beatrix Children's Hospital, Groningen 9700RB, The Netherlands,
the ¶ Department of Genomics and Pathobiology, University of
Alabama at Birmingham, Birmingham, Alabama 35294-0019, the
Department of Cellular Biochemistry, Hannah Research Institute,
Ayr KA6 5HL, Scotland, United Kingdom, the ** Department of
Medical Genetics, University of Groningen, Groningen 9700RB, The
Netherlands, and the Department of Medical
Biology, Molecular Biology Unit, University of Groningen, Groningen
9700RB, The Netherlands
-oxidation of long-chain fatty acids in the heart and skeletal
muscle. Because knowledge of the mammalian genes encoding M-CPT I may
aid in studies of disturbed energy metabolism, we obtained new genomic
and cDNA data for M-CPT I for the human, mouse, rat, and sheep. The
introns of these compact genes are 80% (mouse versus rat)
and 60% (mouse versus human) identical. Sheep and goat,
but not cow, pig, rodent, or human promoter sequences contain a short
interspersed repeated sequence (SINE) upstream of highly conserved
regulatory elements. These elements constitute two promoters in humans,
sheep, and mice, and, contrary to previous reports, there is a second
promoter in rats as well. Thus, the transcriptional organization of
these genes is more uniform than previously supposed, with interspecies differences in the 5'-ends of the mRNAs reflecting differences in
splicing; only in humans extensive splicing and splice variation is
found in the 5'- and 3'-untranslated regions. In the mouse, intron
retention was detected in heart, muscle, and testes and may indicate an
additional mechanism of regulation of M-CPT I expression. Splice
variation in the coding region was previously proposed to lead to
expression of CPT I enzymes with altered malonyl-CoA sensitivity (Yu,
G. S., Lu, Y. C., and Gulick, T. (1998) Biochem. J. 334, 225-231). However, when expressed in the yeast
Pichia pastoris, none of three earlier described splice
variants had CPT I activity. Therefore, the involvement of splice
variation of M-CPT I in the modulation of malonyl-CoA inhibition of
fatty acid oxidation may be less relevant than hitherto assumed.
*
This work was supported by the Netherlands Heart Foundation
(NHS 97.093 and NHS 2001.081), National Institutes of Health Grant RO1-RR-02599, the Scottish Executive Environment and Rural Affairs Department, and the British Heart Foundation.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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