Low translational efficiency of the F1‐ATPase β‐subunit mRNA largely accounts for the decreased ATPase content in brown adipose tissue mitochondria

Abstract
The half‐life of the F1‐ATPase β‐subunit (F1‐β) mRNA in ATPase‐poor brown adipose tissue (BAT) (t?? = 9.5 h) was found to be 3–7‐fold shorter than in liver (t?? = 27 h) and heart (t?? = 63 h) of mice. When translated in reticulocyte lysate, a 2–3‐fold lower efficiency appeared with F1‐β mRNA from BAT than from other tissues. The in vitro synthesized F1‐β 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 or abundant F1‐β mRNA in BAT is not fully translatable most likely due to its low metabolic stability.