Gangming Zhang
Shaoyu Lin
Juanming Shi
Hong Zhang
Junjie Hu
1 National Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China;
2 Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin 300071, China;
3 Programs in Biomedical and Biological Sciences, University of Southern California, Los Angeles, CA 90089, USA
Funds: We thank Dr. Jun Zhou for reagents and help with microtubule sedimentation assay, Dr. Gert Kreibich for M3/18 cells, Dr. Dong Li for mEmerald-Ensconsin plasmid and Xin Zhou and Fang Chen for technical assistance. J.H. is supported by the National Key Research and Development Program (Grant No. 2016YFA0500201), the National Natural Science Foundation of China (Grant Nos. 31225006 and 31421002), and an International Early Career Scientist grant from Howard Hughes Medical Institute.
Received Date: 2017-10-11
Rev Recd Date:2017-11-13
Abstract
Abstract
Sec61β, a subunit of the Sec61 translocon complex, is not essential in yeast and commonly used as a marker of endoplasmic reticulum (ER). In higher eukaryotes, such as Drosophila, deletion of Sec61β causes lethality, but its physiological role is unclear. Here, we show that Sec61β interacts directly with microtubules. Overexpression of Sec61β containing small epitope tags, but not a RFP tag, induces dramatic bundling of the ER and microtubule. A basic region in the cytosolic domain of Sec61β is critical for microtubule association. Depletion of Sec61β induces ER stress in both mammalian cells and Caenorhabditis elegans, and subsequent restoration of ER homeostasis correlates with the microtubule binding ability of Sec61β. Loss of Sec61β causes increased mobility of translocon complexes and reduced level of membrane-bound ribosomes. These results suggest that Sec61β may stabilize protein translocation by linking translocon complex to microtubule and provide insight into the physiological function of ER-microtubule interaction.Keywords: ER stress,
Microtubule,
Sec61β,
Translocon,
Ribosome
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