Arunachalam Easun, Keber Felix C, Law Richard C, Kumar Chirag K, Shen Yihui, Park Junyoung O, Wühr Martin, Needleman Daniel J
Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA, USA.
Lewis-Sigler Institute for Integrative Genomics.
bioRxiv. 2024 Jul 5:2024.07.04.601975. doi: 10.1101/2024.07.04.601975.
A long-standing observation is that in fast-growing cells, respiration rate declines with increasing growth rate and is compensated by an increase in fermentation, despite respiration being more efficient than fermentation. This apparent preference for fermentation even in the presence of oxygen is known as aerobic glycolysis, and occurs in bacteria, yeast, and cancer cells. Considerable work has focused on understanding the potential benefits that might justify this seemingly wasteful metabolic strategy, but its mechanistic basis remains unclear. Here we show that aerobic glycolysis results from the saturation of mitochondrial respiration and the decoupling of mitochondrial biogenesis from the production of other cellular components. Respiration rate is insensitive to acute perturbations of cellular energetic demands or nutrient supplies, and is explained simply by the amount of mitochondria per cell. Mitochondria accumulate at a nearly constant rate across different growth conditions, resulting in mitochondrial amount being largely determined by cell division time. In contrast, glucose uptake rate is not saturated, and is accurately predicted by the abundances and affinities of glucose transporters. Combining these models of glucose uptake and respiration provides a quantitative, mechanistic explanation for aerobic glycolysis. The robustness of specific respiration rate and mitochondrial biogenesis, paired with the flexibility of other bioenergetic and biosynthetic fluxes, may play a broad role in shaping eukaryotic cell metabolism.
长期以来的观察结果是,在快速生长的细胞中,呼吸速率会随着生长速率的增加而下降,并通过发酵作用的增强来补偿,尽管呼吸作用比发酵作用更高效。即使在有氧存在的情况下,这种对发酵作用的明显偏好也被称为有氧糖酵解,它在细菌、酵母和癌细胞中都会发生。大量研究致力于理解这种看似浪费的代谢策略可能带来的潜在益处,但其机制基础仍不清楚。在这里,我们表明有氧糖酵解是由线粒体呼吸的饱和以及线粒体生物发生与其他细胞成分产生的解偶联所导致的。呼吸速率对细胞能量需求或营养供应的急性扰动不敏感,并且仅由每个细胞中的线粒体数量来解释。线粒体在不同生长条件下以几乎恒定的速率积累,导致线粒体数量在很大程度上由细胞分裂时间决定。相比之下,葡萄糖摄取速率并未饱和,并且可以通过葡萄糖转运蛋白的丰度和亲和力准确预测。结合这些葡萄糖摄取和呼吸的模型,为有氧糖酵解提供了定量的、机制性的解释。特定呼吸速率和线粒体生物发生的稳健性,与其他生物能量和生物合成通量的灵活性相结合,可能在塑造真核细胞代谢中发挥广泛作用。