Clearance and adaptation to reactive oxygen species (ROS) are crucial for cell survival. As in other eukaryotes, the Neurospora catalases are the main enzymes responsible for ROS clearance and their expression are tightly regulated by the growth and environmental conditions. The RNA polymerase II carboxyl terminal domain (RNAPII CTD) kinase complex (CTK complex) is known as a positive elongation factor for many inducible genes by releasing paused RNAPII near the transcription start site and promoting transcription elongation. However, here we show that deletion of CTK complex components in Neurospora led to high CAT-3 expression level and resistance to H2 O2 -induced ROS stress. The catalytic activity of CTK-1 is required for such a response. On the other hand, CTK-1 overexpression led to decreased expression of CAT-3. ChIP assays shows that CTK-1 phosphorylates the RNAPII CTD at Ser2 residues in the cat-3 ORF region during transcription elongation and deletion of CTK-1 led to dramatic decreases of SET-2 recruitment and H3K36me3 modification. As a result, histones at the cat-3 locus become hyperacetylated to promote its transcription. Together, these results demonstrate that the CTK complex is negative regulator of cat-3 expression by affecting its chromatin structure.

中文翻译：

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Neurospora RNA聚合酶II激酶CTK以染色质上下文相关的方式负调节过氧化氢酶的表达。

清除和适应活性氧（ROS）对于细胞存活至关重要。与其他真核生物一样，神经孢子过氧化氢酶是负责清除ROS的主要酶，其表达受到生长和环境条件的严格调控。通过在转录起始位点附近释放暂停的RNAPII并促进转录延伸，RNA聚合酶II羧基末端域（RNAPII CTD）激酶复合物（CTK复合物）被称为许多可诱导基因的正延伸因子。但是，这里我们显示，神经孢菌中CTK复杂成分的缺失导致高CAT-3表达水平和对H2 O2诱导的ROS胁迫的抵抗力。这种反应需要CTK-1的催化活性。另一方面，CTK-1的过表达导致CAT-3的表达降低。ChIP分析表明，在转录延长和CTK-1缺失导致SET-2募集和H3K36me3修饰显着降低的过程中，CTK-1使cat-3 ORF区中Ser2残基处的RNAPII CTD磷酸化。结果，cat-3基因座的组蛋白变得高度乙酰化，从而促进其转录。总之，这些结果表明，CTK复合物通过影响其染色质结构而成为cat-3表达的负调节剂。