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通过将核孔蛋白异位靶向染色质来分析核孔组装的起始。

Analysis of the initiation of nuclear pore assembly by ectopically targeting nucleoporins to chromatin.

作者信息

Schwartz Michal, Travesa Anna, Martell Steven W, Forbes Douglass J

机构信息

a Section of Cell and Developmental Biology; Division of Biological Sciences 0347; University of California-San Diego ; La Jolla , CA USA.

出版信息

Nucleus. 2015;6(1):40-54. doi: 10.1080/19491034.2015.1004260.

Abstract

Nuclear pore complexes (NPCs) form the gateway to the nucleus, mediating virtually all nucleocytoplasmic trafficking. Assembly of a nuclear pore complex requires the organization of many soluble sub-complexes into a final massive structure embedded in the nuclear envelope. By use of a LacI/LacO reporter system, we were able to assess nucleoporin (Nup) interactions, show that they occur with a high level of specificity, and identify nucleoporins sufficient for initiation of the complex process of NPC assembly in vivo. Eleven nucleoporins from different sub-complexes were fused to LacI-CFP and transfected separately into a human cell line containing a stably integrated LacO DNA array. The LacI-Nup fusion proteins, which bound to the array, were examined for their ability to recruit endogenous nucleoporins to the intranuclear LacO site. Many could recruit nucleoporins of the same sub-complex and a number could also recruit other sub-complexes. Strikingly, Nup133 and Nup107 of the Nup107/160 subcomplex and Nup153 and Nup50 of the nuclear pore basket recruited a near full complement of nucleoporins to the LacO array. Furthermore, Nup133 and Nup153 efficiently targeted the LacO array to the nuclear periphery. Our data support a hierarchical, seeded assembly pathway and identify Nup133 and Nup153 as effective "seeds" for NPC assembly. In addition, we show that this system can be applied to functional studies of individual nucleoporin domains as well as to specific nucleoporin disease mutations. We find that the R391H cardiac arrhythmia/sudden death mutation of Nup155 prevents both its subcomplex assembly and nuclear rim targeting of the LacO array.

摘要

核孔复合体(NPCs)构成了进入细胞核的通道,几乎介导了所有的核质运输。核孔复合体的组装需要将许多可溶性亚复合体组织成一个嵌入核膜的最终大型结构。通过使用LacI/LacO报告系统,我们能够评估核孔蛋白(Nup)之间的相互作用,表明它们以高度特异性发生,并确定在体内启动NPC组装复杂过程所需的核孔蛋白。来自不同亚复合体的11种核孔蛋白与LacI-CFP融合,并分别转染到含有稳定整合的LacO DNA阵列的人细胞系中。检查与阵列结合的LacI-Nup融合蛋白将内源性核孔蛋白募集到核内LacO位点的能力。许多融合蛋白可以募集同一亚复合体的核孔蛋白,一些还可以募集其他亚复合体的核孔蛋白。引人注目的是,Nup107/160亚复合体的Nup133和Nup107以及核孔篮的Nup153和Nup50将几乎完整的核孔蛋白补充物募集到LacO阵列。此外,Nup133和Nup153有效地将LacO阵列靶向核周边。我们的数据支持一种分级的、种子式组装途径,并确定Nup133和Nup153是NPC组装的有效“种子”。此外,我们表明该系统可应用于单个核孔蛋白结构域的功能研究以及特定的核孔蛋白疾病突变研究。我们发现Nup155的R391H心律失常/猝死突变既阻止了其亚复合体组装,也阻止了LacO阵列的核边缘靶向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e22/4615246/cdb7324630e1/kncl-06-01-1004260-g001.jpg

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