National Heart Lung and Blood Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20814, USA
Department of Zoology, University of British Columbia, 6270 University Blvd, Vancouver, British Columbia, Canada V6T 1Z4.
J Exp Biol. 2020 Oct 27;223(Pt 20):jeb227801. doi: 10.1242/jeb.227801.
Temperature is a critical abiotic factor shaping the distribution and abundance of species, but the mechanisms that underpin organismal thermal limits remain poorly understood. One possible mechanism underlying these limits is the failure of mitochondrial processes, as mitochondria play a crucial role in animals as the primary site of ATP production. Conventional measures of mitochondrial performance suggest that these organelles can function at temperatures much higher than those that limit whole-organism function, suggesting that they are unlikely to set organismal thermal limits. However, this conclusion is challenged by recent data connecting sequence variation in mitochondrial genes to whole-organism thermal tolerance. Here, we review the current state of knowledge of mitochondrial responses to thermal extremes and ask whether they are consistent with a role for mitochondrial function in shaping whole-organism thermal limits. The available data are fragmentary, but it is possible to draw some conclusions. There is little evidence that failure of maximal mitochondrial oxidative capacity as assessed sets thermal limits, but there is some evidence to suggest that temperature effects on ATP synthetic capacity may be important. Several studies suggest that loss of mitochondrial coupling is associated with the thermal limits for organismal growth, although this needs to be rigorously tested. Most studies have utilized isolated mitochondrial preparations to assess the effects of temperature on these organelles, and there remain many untapped opportunities to address these questions using preparations that retain more of their biological context to better connect these subcellular processes with whole-organism thermal limits.
温度是塑造物种分布和丰度的关键非生物因素,但支撑生物热极限的机制仍知之甚少。这些限制的一个可能机制是线粒体过程的失败,因为线粒体在动物中作为 ATP 产生的主要场所起着至关重要的作用。线粒体性能的常规测量表明,这些细胞器可以在远高于限制整个生物体功能的温度下发挥作用,这表明它们不太可能设定生物体的热极限。然而,最近将线粒体基因序列变异与整个生物体热耐受性联系起来的数据对这一结论提出了挑战。在这里,我们回顾了线粒体对热极端反应的现有知识状态,并询问它们是否与线粒体功能在塑造整个生物体热极限中的作用一致。可用的数据是零碎的,但可以得出一些结论。几乎没有证据表明最大线粒体氧化能力的衰竭(如通过评估得出)设定了热极限,但有一些证据表明,温度对 ATP 合成能力的影响可能很重要。几项研究表明,线粒体偶联的丧失与生物体生长的热极限有关,尽管这需要严格测试。大多数研究都利用分离的线粒体制剂来评估温度对这些细胞器的影响,但仍有许多未开发的机会来利用更能保留其生物学背景的制剂来解决这些问题,从而将这些亚细胞过程与整个生物体的热极限更好地联系起来。