Expression and sequence analysis of the mouse adenine nucleotide translocase 1 and 2 genes

Citation
Se. Levy et al., Expression and sequence analysis of the mouse adenine nucleotide translocase 1 and 2 genes, GENE, 254(1-2), 2000, pp. 57-66
Citations number
33
Categorie Soggetti
Molecular Biology & Genetics
Journal title
GENE
ISSN journal
03781119 → ACNP
Volume
254
Issue
1-2
Year of publication
2000
Pages
57 - 66
Database
ISI
SICI code
0378-1119(20000822)254:1-2<57:EASAOT>2.0.ZU;2-1
Abstract
Only two isoforms of the adenine nucleotide translocase (Ant) protein have been identified in mouse, as opposed to the three in humans. To determine w hether the homologous mouse and human proteins share similar patterns of ex pression, Northern and Western analyses were performed on several mouse tis sues. Mouse Ant1 is expressed at high levels in skeletal muscle and heart, similar to human ANT1. Mouse Ant2 is strongly expressed in all tissues but muscle, in marked contrast to human ANT2. To investigate the molecular basi s of these differences, we cloned and sequenced the genomic loci of mouse A nt1 and Ant2, and compared them to the three human ANT loci. The mouse and human ANT1 and ANT2 genes showed substantial homology starting about 300 ba se pairs (bp) 5' to the coding region and continuing through the 3' untrans lated region (UTR). Repeats constituted 32% of 15 kb of Ant1 sequence and 3 6% of the 27 kb of Ant2 sequence and included SINEs, LINEs and LTR elements . The core promoters of the mouse and human ANT1 and ANT2 genes are very si milar. However, the mouse Anti gene lacks the upstream OXBOX and REBOX elem ents found in human ANT1 genes, thought to be important for muscle-specific expression. The mouse Ant2 gene, like human ANT2, has an upstream GRBOX, y et this element is not associated with suppression of transcription, as hyp othesized for human ANT2. These discrepancies indicate that additional stud ies will be required to fully understand the transcriptional regulation of both Ant1 and Ant2. (C) 2000 Published by Elsevier Science B.V. All rights reserved.