Temperature regulates splicing efficiency of the cold-inducible RNA-binding protein gene Cirbp.
Temperature regulates splicing efficiency of the cold-inducible RNA-binding protein gene Cirbp.
复制标题
温度调节可冷诱导的RNA结合蛋白基因CIRBP的剪接效率。
DOI：
10.1101/gad.287094.116
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发表时间：
2016-09-01
影响因子：
10.5
通讯作者：
Schibler U
中科院分区：
文献类型：
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作者：
Gotic I;Omidi S;Fleury-Olela F;Molina N;Naef F;Schibler U
Gotic等人的研究表明，冷诱导rna结合蛋白（Cirbp） mRNA的温度依赖性积累主要受剪接效率的调控。正如全基因组“接近稳态”动力学所揭示的那样，这种转录后机制在温度依赖的基因表达控制中广泛存在。哺乳动物的体温每天在36°C - 37°C的平均值上下波动。尽管最小值和最大值之间的差异很小，但体温节律可以驱动培养细胞（可能也包括动物）中基因表达的强劲周期。在这里，我们研究了冷诱导rna结合蛋白（CIRBP）的温度依赖性表达机制。在暴露于模拟小鼠体温周期的NIH3T3成纤维细胞中，Cirbp mRNA的丰度振荡约为小鼠肝脏的三倍。这种每日mRNA积累周期直接由温度振荡控制，而不依赖于细胞的生物钟。在这里，我们发现Cirbp mRNA的温度依赖性积累主要由剪接效率的调节控制，剪接效率被定义为Cirbp pre-mRNA加工成成熟mRNA的比例。正如全基因组“接近稳态”动力学所揭示的那样，这种转录后机制在温度依赖的基因表达控制中广泛存在。
Gotic et al. show that the temperature-dependent accumulation of cold-inducible RNA-binding protein (Cirbp) mRNA is controlled primarily by the regulation of splicing efficiency. As revealed by genome-wide “approach-to-steady-state” kinetics, this post-transcriptional mechanism is widespread in the temperature-dependent control of gene expression. In mammals, body temperature fluctuates diurnally around a mean value of 36°C–37°C. Despite the small differences between minimal and maximal values, body temperature rhythms can drive robust cycles in gene expression in cultured cells and, likely, animals. Here we studied the mechanisms responsible for the temperature-dependent expression of cold-inducible RNA-binding protein (CIRBP). In NIH3T3 fibroblasts exposed to simulated mouse body temperature cycles, Cirbp mRNA oscillates about threefold in abundance, as it does in mouse livers. This daily mRNA accumulation cycle is directly controlled by temperature oscillations and does not depend on the cells’ circadian clocks. Here we show that the temperature-dependent accumulation of Cirbp mRNA is controlled primarily by the regulation of splicing efficiency, defined as the fraction of Cirbp pre-mRNA processed into mature mRNA. As revealed by genome-wide “approach to steady-state” kinetics, this post-transcriptional mechanism is widespread in the temperature-dependent control of gene expression.