Low translational efficiency of the F1-ATPase beta-subunit mRNA largely accounts for the decreased ATPase content in brown adipose tissue mitochondria
Language English Country England, Great Britain Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
1426264
DOI
10.1016/0014-5793(92)81175-l
PII: 0014-5793(92)81175-L
Knihovny.cz E-resources
- MeSH
- Adenosine Triphosphatases genetics metabolism MeSH
- Adipose Tissue, Brown enzymology MeSH
- Mitochondria, Liver enzymology MeSH
- RNA, Messenger genetics MeSH
- Mitochondria enzymology MeSH
- Myocardium enzymology MeSH
- Mice, Inbred BALB C MeSH
- Mice MeSH
- Blotting, Northern MeSH
- Protein Processing, Post-Translational MeSH
- Protein Precursors metabolism MeSH
- Protein Biosynthesis * MeSH
- Proton-Translocating ATPases genetics MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Adenosine Triphosphatases MeSH
- RNA, Messenger MeSH
- Protein Precursors MeSH
- Proton-Translocating ATPases MeSH
The half-life of the F1-ATPase beta-subunit (F1-beta) mRNA in ATPase-poor brown adipose tissue (BAT) (t1/2 = 9.5 h) was found to be 3-7-fold shorter than in liver (t1/2 = 27 h) and heart (t1/2 = 63 h) of mice. When translated in reticulocyte lysate, a 2-3-fold lower efficiency appeared with F1-beta mRNA from BAT than from other tissues. The in vitro synthesized F1-beta protein precursors of BAT, liver and heart origin were imported and processed by mouse liver mitochondria with equal efficiency. The results indicate that the pool of abundant F1-beta mRNA in BAT is not fully translatable, most likely due to its low metabolic stability.
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