生物体为了生存而必然释放热能。这个过程被称为细胞生热作用，与从癌症代谢到自发农场火灾的许多过程有关。然而，这一基本现象的分子基础尚未阐明。在这里，我们证明参与大肠杆菌细胞产热的主要参与者是蛋白激酶 ArcB、GlnL 和 YccC。我们还揭示了三磷酸腺苷（ATP）驱动的自磷酸化的底物水平控制，该自磷酸化控制着细胞生热作用。具体来说，通过活细胞微量热法，我们发现这些调节蛋白在模型大肠杆菌菌株中被敲除时，会失调细胞生热作用。这种失调可以从这些细胞的热量输出平均增加 25% 或更高中看出。我们还发现，在生长的对数后期，热量输出和细胞内 ATP 水平都达到最大值。此外，我们表明可以通过过度表达 glnL 来改造微生物生热作用。我们的结果证明了细胞中 ATP 浓度与细胞产生多余热量的能力之间的相关性。我们希望这项工作成为工程热原调节生物体用于各种应用的基础。版权所有：© 2023 Dhatt 等人。这是一篇根据知识共享署名许可条款分发的开放获取文章，允许在任何媒体上不受限制地使用、分发和复制，前提是注明原始作者和来源。

Organisms necessarily release heat energy in their pursuit of survival. This process is known as cellular thermogenesis and is implicated in many processes from cancer metabolism to spontaneous farm fires. However, the molecular basis for this fundamental phenomenon is yet to be elucidated. Here, we show that the major players involved in the cellular thermogenesis of Escherichia coli are the protein kinases ArcB, GlnL, and YccC. We also reveal the substrate-level control of adenosine triphosphate (ATP)-driven autophosphorylation that governs cellular thermogenesis. Specifically, through live cell microcalorimetry, we find these regulatory proteins, when knocked out in a model E. coli strain, dysregulate cellular thermogenesis. This dysregulation can be seen in an average 25% or greater increase in heat output by these cells. We also discover that both heat output and intracellular ATP levels are maximal during the late log phase of growth. Additionally, we show that microbial thermogenesis can be engineered through overexpressing glnL. Our results demonstrate a correlation between ATP concentrations in the cell and a cell's ability to generate excess heat. We expect this work to be the foundation for engineering thermogenically tuned organisms for a variety of applications.Copyright: © 2023 Dhatt et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.