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首页> 外文期刊>Nucleic Acids Research >A crucial RNA-binding lysine residue in the Nab3 RRM domain undergoes SET1 and SET3-responsive methylation
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A crucial RNA-binding lysine residue in the Nab3 RRM domain undergoes SET1 and SET3-responsive methylation

机译：NAB3 RRM结构域中的至关重要的RNA结合赖氨酸残基经历SET1和SET3响应甲基化

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摘要

The Nrd1-Nab3-Sent (NNS) complex integrates molecular cues to direct termination of noncoding transcription in budding yeast. NNS is positively regulated by histone methylation as well as through Nrd1 binding to the initiating form of RNA Polll. These cues collaborate with Nrd1 and Nab3 binding to target RNA sequences in nascent transcripts through their RRM RNA recognition motifs. In this study, we identify nine lysine residues distributed amongst Nrd1, Nab3 and Sent that are methylated, suggesting novel molecular inputs for NNS regulation. We identify mono-methylation of one these residues (Nab3-K363me1 ) as being partly dependent on the H3K4 methyltransferase, Sett, a known regulator of NNS function. Moreover, the accumulation of Nab3-K363me1 is essentially abolished in strains lacking SET3, a SET domain containing protein that is positively regulated by H3K4 methylation. Nab3-K363 resides within its RRM and physically contacts target RNA. Mutation of Nab3-K363 to arginine (Nab3-K363R) decreases RNA binding of the Nab3 RRM in vitro and causes transcription termination defects and slow growth. These findings identify SET3 as a potential contextual regulator of Nab3 function through its role in methylation of Nab3-K363. Consistent with this hypothesis, we report that SET3 exhibits genetic activation of NAB3 that is observed in a sensitized context.
机译：NRD1-NAB3送（NNS）复合物整合分子提示以直接终止萌芽酵母中的非编码转录。 NNS由组蛋白甲基化以及通过NRD1与RNA Poll1的引发形式的结合阳性调节。这些提示通过其RRM RNA识别基序与NRD1和NAB3结合到NSCENCE转录物中的RNA序列。在这项研究中，我们鉴定了NRD1，NAB3中的九个赖氨酸残基，并寄出的甲基化，表明NNS调节的新型分子投入。我们将其中一种残留物（Nab3-K363ME1）的单甲基化鉴定为部分依赖于H3K4甲基转移酶，SENT，NNS功能的已知调节剂。此外，NAB3-K363ME1的累积基本上废除缺乏SET3的菌株，含有含有H3K4甲基化的含有正调节的蛋白质的设定结构域。 NAB3-K363驻留在其RRM内，物理接触目标RNA。 NAB3-K363至精氨酸（NAB3-K363R）的突变降低了NAB3 RRM在体外的RNA结合，并导致转录终止缺陷和生长缓慢。这些发现通过其在Nab3-K363的甲基化中的作用识别Set3作为NAB3功能的潜在上下文调节剂。与该假设一致，我们报告该Set3表现出在敏化背景下观察到的NAB3的遗传活化。

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