Cell-autonomous control of intracellular temperature by unsaturation of phospholipid acyl chains
Cell-autonomous control of intracellular temperature by unsaturation of phospholipid acyl chains
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DOI：
10.1016/j.celrep.2022.110487
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发表时间：
2022-03-15
期刊：
影响因子：
8.8
通讯作者：
Umeda, Masato
中科院分区：
文献类型：
--
作者：
Murakami, Akira;Nagao, Kohjiro;Umeda, Masato
细胞内温度影响着生物体内广泛的细胞功能。然而，目前尚不清楚单个动物细胞中的温度是否作为对环境温度波动的反应而自动控制。使用两个不同的细胞内温度计，我们发现稳定状态的果蝇S2细胞的细胞内温度是以一种依赖于Delta 9-脂肪酸去饱和酶DESAT1的方式维持的，DESAT1在酰基CoA的酰基部分的Delta 9位引入了一个双键。DESAT1介导的细胞内温度升高是由于依赖F1F0-ATPase的线粒体呼吸增强而引起的，这与产热作用有关。我们还发现，依赖于F1F0-ATPase的线粒体呼吸在冷暴露下通过依赖于DESAT1的线粒体磷脂酰链不饱和来重塑线粒体的脊结构而增强。基于这些发现，我们提出了在环境温度变化过程中细胞内温度控制的细胞自主机制。
Intracellular temperature affects a wide range of cellular functions in living organisms. However, it remains unclear whether temperature in individual animal cells is controlled autonomously as a response to fluctuations in environmental temperature. Using two distinct intracellular thermometers, we find that the intracellular temperature of steady-state Drosophila S2 cells is maintained in a manner dependent on Delta 9-fatty acid desaturase DESAT1, which introduces a double bond at the Delta 9 position of the acyl moiety of acyl-CoA. The DESAT1-mediated increase of intracellular temperature is caused by the enhancement of F1F0-ATPase-dependent mitochondrial respiration, which is coupled with thermogenesis. We also reveal that F1F0-ATPase-dependent mitochondrial respiration is potentiated by cold exposure through the remodeling of mitochondrial cristae structures via DESAT1-dependent unsaturation of mitochondrial phospholipid acyl chains. Based on these findings, we propose a cell-autonomous mechanism for intracellular temperature control during environmental temperature changes.