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mRNA 输出调节因子 DBP5/DDX19、GLE1 或 IPPK 的耗竭，这些因子是 IP6 产生的关键酶，导致细胞质 mRNA 表达的差异改变和特定的细胞缺陷。

Depletion of mRNA export regulator DBP5/DDX19, GLE1 or IPPK that is a key enzyme for the production of IP6, resulting in differentially altered cytoplasmic mRNA expression and specific cell defect.

机构信息

Division of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto, Kyoto, Japan.

Center for Molecular Biology and Genetics, Mie University, Tsu, Mie, Japan.

出版信息

PLoS One. 2018 May 10;13(5):e0197165. doi: 10.1371/journal.pone.0197165. eCollection 2018.

DOI:10.1371/journal.pone.0197165
PMID:29746542
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5945018/
Abstract

DBP5, also known as DDX19, GLE1 and inositol hexakisphosphate (IP6) function in messenger RNA (mRNA) export at the cytoplasmic surface of the nuclear pore complex in eukaryotic cells. DBP5 is a DEAD-box RNA helicase, and its activity is stimulated by interactions with GLE1 and IP6. In addition, these three factors also have unique role(s). To investigate how these factors influenced the cytoplasmic mRNA expression and cell phenotype change, we performed RNA microarray analysis to detect the effect and function of DBP5, GLE1 and IP6 on the cytoplasmic mRNA expression. The expression of some cytoplasmic mRNA subsets (e.g. cell cycle, DNA replication) was commonly suppressed by the knock-down of DBP5, GLE1 and IPPK (IP6 synthetic enzyme). The GLE1 knock-down selectively reduced the cytoplasmic mRNA expression required for mitotic progression, results in an abnormal spindle phenotype and caused the delay of mitotic process. Meanwhile, G1/S cell cycle arrest was observed in DBP5 and IPPK knock-down cells. Several factors that function in immune response were also down-regulated in DBP5 or IPPK knock-down cells. Thereby, IFNβ-1 mRNA transcription evoked by poly(I:C) treatment was suppressed. These results imply that DBP5, GLE1 and IP6 have a conserved and individual function in the cytoplasmic mRNA expression. Variations in phenotype are due to the difference in each function of DBP5, GLE1 and IPPK in intracellular mRNA metabolism.

摘要

DBP5，也称为 DDX19、GLE1 和肌醇六磷酸（IP6），在真核细胞的核孔复合物细胞质表面参与信使 RNA（mRNA）的输出。DBP5 是一种 DEAD 盒 RNA 解旋酶，其活性受 GLE1 和 IP6 相互作用的刺激。此外，这三个因素也具有独特的作用。为了研究这些因素如何影响细胞质 mRNA 的表达和细胞表型变化，我们进行了 RNA 微阵列分析，以检测 DBP5、GLE1 和 IP6 对细胞质 mRNA 表达的影响。一些细胞质 mRNA 亚群（例如细胞周期、DNA 复制）的表达被 DBP5、GLE1 和 IPPK（IP6 合成酶）的敲低共同抑制。GLE1 的敲低选择性地降低了有丝分裂进展所需的细胞质 mRNA 表达，导致异常纺锤体表型，并导致有丝分裂过程延迟。同时，在 DBP5 和 IPPK 敲低的细胞中观察到 G1/S 细胞周期停滞。在 DBP5 或 IPPK 敲低的细胞中，一些参与免疫反应的因子也下调。因此，多聚（I：C）处理引发的 IFNβ-1 mRNA 转录受到抑制。这些结果表明 DBP5、GLE1 和 IP6 在细胞质 mRNA 表达中具有保守和独特的功能。表型的变化是由于 DBP5、GLE1 和 IPPK 在细胞内 mRNA 代谢中的每个功能的差异所致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d7a/5945018/77ccdfd4aee9/pone.0197165.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d7a/5945018/df033f2b36bb/pone.0197165.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d7a/5945018/9fe73cbc89b9/pone.0197165.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d7a/5945018/058ffccdce55/pone.0197165.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d7a/5945018/70663affd96d/pone.0197165.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d7a/5945018/77ccdfd4aee9/pone.0197165.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d7a/5945018/df033f2b36bb/pone.0197165.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d7a/5945018/256f579970dc/pone.0197165.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d7a/5945018/454097438868/pone.0197165.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d7a/5945018/9fe73cbc89b9/pone.0197165.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d7a/5945018/058ffccdce55/pone.0197165.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d7a/5945018/70663affd96d/pone.0197165.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d7a/5945018/77ccdfd4aee9/pone.0197165.g007.jpg

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