生物钟
生物
乙酰化
组蛋白
细胞生物学
转录因子
染色质
组蛋白乙酰转移酶
生物化学
遗传学
基因
作者
Xiao-Lan Liu,Yulin Yang,Yue Hu,Jingjing Wu,Chuqiao Han,Qiaojia Lu,Xiuni Gan,Shaohua Qi,Jinhu Guo,Qun He,Yi Liu,Xiao Liu
出处
期刊:eLife
[eLife Sciences Publications, Ltd.]
日期:2023-04-21
卷期号:12
被引量:4
摘要
Circadian clocks are evolved to adapt to the daily environmental changes under different conditions. The ability to maintain circadian clock functions in response to various stresses and perturbations is important for organismal fitness. Here, we show that the nutrient-sensing GCN2 signaling pathway is required for robust circadian clock function under amino acid starvation in Neurospora. The deletion of GCN2 pathway components disrupts rhythmic transcription of clock gene frq by suppressing WC complex binding at the frq promoter due to its reduced histone H3 acetylation levels. Under amino acid starvation, the activation of GCN2 kinase and its downstream transcription factor CPC-1 establish a proper chromatin state at the frq promoter by recruiting the histone acetyltransferase GCN-5. The arrhythmic phenotype of the GCN2 kinase mutants under amino acid starvation can be rescued by inhibiting histone deacetylation. Finally, genome-wide transcriptional analysis indicates that the GCN2 signaling pathway maintains robust rhythmic expression of metabolic genes under amino acid starvation. Together, these results uncover an essential role of the GCN2 signaling pathway in maintaining the robust circadian clock function in response to amino acid starvation, and demonstrate the importance of histone acetylation at the frq locus in rhythmic gene expression.
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