Journal
GENES & GENETIC SYSTEMS
Volume 84, Issue 5, Pages 327-334Publisher
GENETICS SOC JAPAN
DOI: 10.1266/ggs.84.327
Keywords
intracisternal type A particle element; insertion; glycolysis; high-throughput screening; phosphoglycerate mutase
Funding
- Center of Genomics and Bioinformatics and Center in Connective Tissue Research, at University of Tennessee Health Science Center
- Veterans Administration
- National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health [R01 AR51190, AR051440]
- Muscular Dystrophy Association [3189]
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Intracisternal A-particle retrotransposons (IAPs) are known, moveable, retrovirus-like elements and are defective in envelope protein synthesis in the mouse genome. Insertion of TAP elements can either interupt or enhance gene function or expression. Using a mouse model called lethal wasting (lew), we recently identified the insertion of an TAP sequence in a gene, 9630033F20Rik, that contains domains involved in glycolysis. The expression pattern of the 9630033F20Rik gene between various normal and diseased tissues was determined by semi-quantitative RT-PCR. The effect of the insertion mutation in 9630033F20Rik on glycolysis in heart, muscle, and brain tissues was further investigated using oligonuleotide microarray analysis. Results indicated that the expression of 9630033F20Rik is ubiquitous and its signal is relatively higher in heart and brain tissues. The insertion caused the deletion of exon 5 and decreased expression of this gene in all the tissues studied in the lew mice. Changes in the expression levels of glycolytic genes mainly occured in muscle tissue, raising a possibility that 9630033F20Rik may function as one of the transcriptional regulators of glycolytic genes in skeletal muscle. However, considering the fact that a single nucleotide mutation in vesicle-associated membrane protein 1 (VAMP1) has been reported as the causal gene for the lew mouse, how much of an impact the TAP insertion in the lew mouse phenotype has on glycolytic genes compared to the effect from the VAMP1 mutation responsible for the lew mouse phenotype should be further investigated.
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