Transcriptional repression of frequency by the IEC-1-INO80 complex is required for normal Neurospora circadian clock function
Transcriptional repression of frequency by the IEC-1-INO80 complex is required for normal Neurospora circadian clock function
复制标题
IEC-1-INO80 复合物对频率的转录抑制是正常脉孢菌生物钟功能所必需的
DOI：
10.1371/journal.pgen.1006732
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发表时间：
2017-04-01
期刊：
影响因子：
4.5
通讯作者：
He, Qun
中科院分区：
文献类型：
--
作者：
Gai, Kexin;Cao, Xuemei;He, Qun
频率（frq）基因的节律性激活和抑制对脉孢菌生物钟的正常功能至关重要。白领复合体（白色COLLAR complex，WC）是脉孢菌昼夜节律系统的正性元件，负责刺激frq转录。我们报道了一种含有C2 H2指状结构域的蛋白IEC-1及其相关的染色质重塑复合物INO 80在正常脉孢菌生物钟功能中发挥重要作用。在iec-1 KO菌株中，昼夜节律被消除，并且与野生型菌株相比，frq转录物水平增加。在INO 80亚基的突变株中观察到类似的结果。此外，ChIP数据显示，INO 80复合物向frq启动子的募集是IEC-1依赖性的。WC介导的frq转录有助于在frq启动子处的INO 80复合物的节律结合。如ChIP分析所示，INO 80复合物是在frq启动子处重建致密染色质环境所必需的。此外，不依赖WC的frq转录存在于ino 80突变体中。总之，我们的数据表明，INO 80复合物抑制frq转录后，通过重新组装的抑制机制在frq启动子frq。
Rhythmic activation and repression of the frequency (frq) gene are essential for normal function of the Neurospora circadian clock. WHITE COLLAR (WC) complex, the positive element of the Neurospora circadian system, is responsible for stimulation of frq transcription. We report that a C2H2 finger domain-containing protein IEC-1 and its associated chromatin remodeling complex INO80 play important roles in normal Neurospora circadian clock function. In iec-1KO strains, circadian rhythms are abolished, and the frq transcript levels are increased compared to that of the wild-type strain. Similar results are observed in mutant strains of the INO80 subunits. Furthermore, ChIP data show that recruitment of the INO80 complex to the frq promoter is IEC-1-dependent. WC-mediated transcription of frq contributes to the rhythmic binding of the INO80 complex at the frq promoter. As demonstrated by ChIP analysis, the INO80 complex is required for the re-establishment of the dense chromatin environment at the frq promoter. In addition, WC-independent frq transcription is present in ino80 mutants. Altogether, our data indicate that the INO80 complex suppresses frq transcription by re-assembling the suppressive mechanisms at the frq promoter after transcription of frq.