Prahlad Veena, Cornelius Tyler, Morimoto Richard I
Department of Biochemistry, Molecular Biology, and Cell Biology, Rice Institute for Biomedical Research, Northwestern University, Evanston, IL 60208, USA.
Science. 2008 May 9;320(5877):811-4. doi: 10.1126/science.1156093.
Temperature pervasively affects all cellular processes. In response to a rapid increase in temperature, all cells undergo a heat shock response, an ancient and highly conserved program of stress-inducible gene expression, to reestablish cellular homeostasis. In isolated cells, the heat shock response is initiated by the presence of misfolded proteins and therefore thought to be cell-autonomous. In contrast, we show that within the metazoan Caenorhabditis elegans, the heat shock response of somatic cells is not cell-autonomous but rather depends on the thermosensory neuron, AFD, which senses ambient temperature and regulates temperature-dependent behavior. We propose a model whereby this loss of cell autonomy serves to integrate behavioral, metabolic, and stress-related responses to establish an organismal response to environmental change.
温度广泛影响所有细胞过程。响应温度的快速升高,所有细胞都会经历热休克反应,这是一个古老且高度保守的应激诱导基因表达程序,以重新建立细胞内稳态。在分离的细胞中,热休克反应由错误折叠的蛋白质引发,因此被认为是细胞自主的。相比之下,我们发现,在多细胞动物秀丽隐杆线虫中,体细胞的热休克反应并非细胞自主的,而是依赖于热感觉神经元AFD,该神经元感知环境温度并调节温度依赖性行为。我们提出了一个模型,据此细胞自主性的丧失有助于整合行为、代谢和应激相关反应,以建立生物体对环境变化的反应。