Wellcome Trust Centre for Mitochondrial Research, Institute for Cell and Molecular Biosciences, Newcastle University, Medical School Newcastle upon Tyne, UK.
Front Microbiol. 2014 Jul 18;5:374. doi: 10.3389/fmicb.2014.00374. eCollection 2014.
Protein synthesis is central to life and maintaining a highly accurate and efficient mechanism is essential. What happens when a translating ribosome stalls on a messenger RNA? Many highly intricate processes have been documented in the cytosol of numerous species, but how does organellar protein synthesis resolve this stalling issue? Mammalian mitochondria synthesize just thirteen highly hydrophobic polypeptides. These proteins are all integral components of the machinery that couples oxidative phosphorylation. Consequently, it is essential that stalled mitochondrial ribosomes can be efficiently recycled. To date, there is no evidence to support any particular molecular mechanism to resolve this problem. However, here we discuss the observation that there are four predicted members of the mitochondrial translation release factor family and that only one member, mtRF1a, is necessary to terminate the translation of all thirteen open reading frames in the mitochondrion. Could the other members be involved in the process of recycling stalled mitochondrial ribosomes?
蛋白质合成是生命的核心，维持高度准确和高效的机制是至关重要的。当翻译核糖体在信使 RNA 上停滞时会发生什么？在许多物种的细胞质中已经记录了许多非常复杂的过程，但细胞器蛋白合成如何解决这个停滞问题？哺乳动物线粒体仅合成十三种高度疏水性的多肽。这些蛋白质都是将氧化磷酸化偶联在一起的机器的组成部分。因此，停滞的线粒体核糖体能够有效地回收是至关重要的。迄今为止，没有证据支持任何特定的分子机制来解决这个问题。然而，在这里我们讨论了这样一个观察结果，即线粒体翻译释放因子家族有四个预测成员，而只有一个成员 mtRF1a 是终止线粒体中十三个开放阅读框翻译所必需的。其他成员是否可能参与停滞的线粒体核糖体的回收过程？
