Raghunayakula Sarita, Subramonian Divya, Dasso Mary, Kumar Rita, Zhang Xiang-Dong
Department of Biological Sciences, Wayne State University, Detroit, Michigan, United States of America.
Laboratory of Gene Regulation and Development, National Institute for Child Health and Human Development, NIH, Bethesda, Maryland, United States of America.
PLoS One. 2015 Dec 7;10(12):e0144508. doi: 10.1371/journal.pone.0144508. eCollection 2015.
Annulate lamellae are cytoplasmic organelles containing stacked sheets of membranes embedded with pore complexes. These cytoplasmic pore complexes at annulate lamellae are morphologically similar to nuclear pore complexes at the nuclear envelope. Although annulate lamellae has been observed in nearly all types of cells, their biological functions are still largely unknown. Here we show that SUMO1-modification of the Ran GTPase-activating protein RanGAP1 not only target RanGAP1 to its known sites at nuclear pore complexes but also to annulate lamellae pore complexes through interactions with the Ran-binding protein RanBP2 and the SUMO-conjugating enzyme Ubc9 in mammalian cells. Furthermore, upregulation of annulate lamellae, which decreases the number of nuclear pore complexes and concurrently increases that of annulate lamellae pore complexes, causes a redistribution of nuclear transport receptors including importin α/β and the exportin CRM1 from nuclear pore complexes to annulate lamellae pore complexes and also reduces the rates of nuclear import and export. Moreover, our results reveal that importin α/β-mediated import complexes initially accumulate at annulate lamellae pore complexes upon the activation of nuclear import and subsequently disassociate for nuclear import through nuclear pore complexes in cells with upregulation of annulate lamellae. Lastly, CRM1-mediated export complexes are concentrated at both nuclear pore complexes and annulate lamellae pore complexes when the disassembly of these export complexes is inhibited by transient expression of a Ran GTPase mutant arrested in its GTP-bound form, suggesting that RanGAP1/RanBP2-activated RanGTP hydrolysis at these pore complexes is required for the dissociation of the export complexes. Hence, our findings provide a foundation for further investigation of how upregulation of annulate lamellae decreases the rates of nuclear transport and also for elucidation of the biological significance of the interaction between annulate lamellae pore complexes and nuclear transport complexes in mammalian cells.
环形片层是一种细胞质细胞器,包含堆叠的膜片层,上面镶嵌着孔复合体。环形片层上的这些细胞质孔复合体在形态上与核膜上的核孔复合体相似。尽管在几乎所有类型的细胞中都观察到了环形片层,但其生物学功能仍然很大程度上未知。在这里,我们表明,Ran GTP酶激活蛋白RanGAP1的SUMO1修饰不仅将RanGAP1靶向其在核孔复合体的已知位点,还通过与哺乳动物细胞中的Ran结合蛋白RanBP2和SUMO结合酶Ubc9相互作用,将其靶向环形片层孔复合体。此外,环形片层的上调会减少核孔复合体的数量,同时增加环形片层孔复合体的数量,导致包括输入蛋白α/β和输出蛋白CRM1在内的核转运受体从核孔复合体重新分布到环形片层孔复合体,也会降低核输入和输出的速率。此外,我们的结果表明,在环形片层上调的细胞中,输入蛋白α/β介导的输入复合体在核输入激活后最初在环形片层孔复合体处积累,随后通过核孔复合体解离以进行核输入。最后,当这些输出复合体的解离被以GTP结合形式停滞的Ran GTP酶突变体的瞬时表达抑制时,CRM1介导的输出复合体集中在核孔复合体和环形片层孔复合体上,这表明在这些孔复合体处RanGAP1/RanBP2激活的RanGTP水解是输出复合体解离所必需的。因此,我们的发现为进一步研究环形片层上调如何降低核转运速率以及阐明哺乳动物细胞中环形片层孔复合体与核转运复合体之间相互作用的生物学意义奠定了基础。