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移动晚期内涵体调节外周内质网网络结构。

Mobile late endosomes modulate peripheral endoplasmic reticulum network architecture.

机构信息

Division of Cell and Chemical Biology, Oncode Institute, Leiden University Medical Centre, Leiden, The Netherlands.

出版信息

EMBO Rep. 2021 Mar 3;22(3):e50815. doi: 10.15252/embr.202050815. Epub 2021 Feb 8.

Abstract

The endoplasmic reticulum (ER) is the largest organelle contacting virtually every other organelle for information exchange and control of processes such as transport, fusion, and fission. Here, we studied the role of the other organelles on ER network architecture in the cell periphery. We show that the co-migration of the ER with other organelles, called ER hitchhiking facilitated by late endosomes and lysosomes is a major mechanism controlling ER network architecture. When hitchhiking occurs, emerging ER structures may fuse with the existing ER tubules to alter the local ER architecture. This couples late endosomal/lysosomal positioning and mobility to ER network architecture. Conditions restricting late endosomal movement-including cell starvation-or the depletion of tether proteins that link the ER to late endosomes reduce ER dynamics and limit the complexity of the peripheral ER network architecture. This indicates that among many factors, the ER is controlled by late endosomal movement resulting in an alteration of the ER network architecture.

摘要

内质网(ER)是与几乎所有其他细胞器接触的最大细胞器,用于信息交换和控制运输、融合和裂变等过程。在这里,我们研究了其他细胞器在细胞外周 ER 网络结构中的作用。我们表明,内质网与其他细胞器的共同迁移,称为晚期内体和溶酶体介导的 ER 搭便车,是控制 ER 网络结构的主要机制。当搭便车发生时,新出现的 ER 结构可能与现有的 ER 小管融合,从而改变局部 ER 结构。这将晚期内体/溶酶体的定位和迁移与 ER 网络结构联系起来。限制晚期内体运动的条件,包括细胞饥饿,或连接 ER 和晚期内体的 tether 蛋白的耗竭,会降低 ER 的动态性,并限制外围 ER 网络结构的复杂性。这表明,在许多因素中,ER 受晚期内体运动的控制,导致 ER 网络结构的改变。

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