Xu, F., Du, W., Zou, Q., Wang, Y., Zhang, X., Xing, X., Li, Y., Zhang, D., Wang, H., Zhang, W., Hu, X., Liu, X., Liu, X., Zhang, S., Yu, J., Fang, J., Li, F., Zhou, Y., Yue, T., ... Yu, L. (2021). COPII mitigates ER stress by promoting formation of ER whorls. Cell Research, 31(2), 141-156. https://doi.org/10.1038/s41422-020-00416-2
Xu, Fang ; Du, Wanqing ; Zou, Qin et al. / COPII mitigates ER stress by promoting formation of ER whorls. In: Cell Research. 2021 ; Vol. 31, No. 2. pp. 141-156.
@article{951608e2526c40169b2cdcfc4c490173,
title = "COPII mitigates ER stress by promoting formation of ER whorls",
abstract = "Cells mitigate ER stress through the unfolded protein response (UPR). Here, we report formation of ER whorls as an effector mechanism of the ER stress response. We found that strong ER stress induces formation of ER whorls, which contain ER-resident proteins such as the Sec61 complex and PKR-like ER kinase (PERK). ER whorl formation is dependent on PERK kinase activity and is mediated by COPII machinery, which facilitates ER membrane budding to form tubular-vesicular ER whorl precursors. ER whorl precursors then go through Sec22b-mediated fusion to form ER whorls. We further show that ER whorls contribute to ER stress-induced translational inhibition by possibly modulating PERK activity and by sequestering translocons in a ribosome-free environment. We propose that formation of ER whorls reflects a new type of ER stress response that controls inhibition of protein translation.",
author = "Fang Xu and Wanqing Du and Qin Zou and Yuting Wang and Xin Zhang and Xudong Xing and Ying Li and Dachuan Zhang and Huimin Wang and Wenhao Zhang and Xinyao Hu and Xin Liu and Xiaoling Liu and Shaojin Zhang and Jinqiang Yu and Jianhuo Fang and Fajin Li and Ying Zhou and Tieqiang Yue and Na Mi and Haiteng Deng and Peng Zou and Xiaowei Chen and Xuerui Yang and Li Yu",
note = "Publisher Copyright: {\textcopyright} 2020, The Author(s).",
year = "2021",
month = feb,
doi = "10.1038/s41422-020-00416-2",
language = "English",
volume = "31",
pages = "141--156",
journal = "Cell Research",
issn = "1001-0602",
publisher = "Springer Nature",
number = "2",
}
Xu, F, Du, W, Zou, Q, Wang, Y, Zhang, X, Xing, X, Li, Y, Zhang, D, Wang, H, Zhang, W, Hu, X, Liu, X, Liu, X, Zhang, S, Yu, J, Fang, J, Li, F, Zhou, Y, Yue, T, Mi, N, Deng, H, Zou, P, Chen, X, Yang, X & Yu, L 2021, 'COPII mitigates ER stress by promoting formation of ER whorls', Cell Research, vol. 31, no. 2, pp. 141-156. https://doi.org/10.1038/s41422-020-00416-2
COPII mitigates ER stress by promoting formation of ER whorls. / Xu, Fang; Du, Wanqing
; Zou, Qin et al.
In:
Cell Research, Vol. 31, No. 2, 02.2021, p. 141-156.
Research output: Contribution to journal › Article › peer-review
TY - JOUR
T1 - COPII mitigates ER stress by promoting formation of ER whorls
AU - Xu, Fang
AU - Du, Wanqing
AU - Zou, Qin
AU - Wang, Yuting
AU - Zhang, Xin
AU - Xing, Xudong
AU - Li, Ying
AU - Zhang, Dachuan
AU - Wang, Huimin
AU - Zhang, Wenhao
AU - Hu, Xinyao
AU - Liu, Xin
AU - Liu, Xiaoling
AU - Zhang, Shaojin
AU - Yu, Jinqiang
AU - Fang, Jianhuo
AU - Li, Fajin
AU - Zhou, Ying
AU - Yue, Tieqiang
AU - Mi, Na
AU - Deng, Haiteng
AU - Zou, Peng
AU - Chen, Xiaowei
AU - Yang, Xuerui
AU - Yu, Li
N1 - Publisher Copyright:
© 2020, The Author(s).
PY - 2021/2
Y1 - 2021/2
N2 - Cells mitigate ER stress through the unfolded protein response (UPR). Here, we report formation of ER whorls as an effector mechanism of the ER stress response. We found that strong ER stress induces formation of ER whorls, which contain ER-resident proteins such as the Sec61 complex and PKR-like ER kinase (PERK). ER whorl formation is dependent on PERK kinase activity and is mediated by COPII machinery, which facilitates ER membrane budding to form tubular-vesicular ER whorl precursors. ER whorl precursors then go through Sec22b-mediated fusion to form ER whorls. We further show that ER whorls contribute to ER stress-induced translational inhibition by possibly modulating PERK activity and by sequestering translocons in a ribosome-free environment. We propose that formation of ER whorls reflects a new type of ER stress response that controls inhibition of protein translation.
AB - Cells mitigate ER stress through the unfolded protein response (UPR). Here, we report formation of ER whorls as an effector mechanism of the ER stress response. We found that strong ER stress induces formation of ER whorls, which contain ER-resident proteins such as the Sec61 complex and PKR-like ER kinase (PERK). ER whorl formation is dependent on PERK kinase activity and is mediated by COPII machinery, which facilitates ER membrane budding to form tubular-vesicular ER whorl precursors. ER whorl precursors then go through Sec22b-mediated fusion to form ER whorls. We further show that ER whorls contribute to ER stress-induced translational inhibition by possibly modulating PERK activity and by sequestering translocons in a ribosome-free environment. We propose that formation of ER whorls reflects a new type of ER stress response that controls inhibition of protein translation.
UR - http://www.scopus.com/inward/record.url?scp=85091612039&partnerID=8YFLogxK
U2 - 10.1038/s41422-020-00416-2
DO - 10.1038/s41422-020-00416-2
M3 - Article
C2 - 32989223
AN - SCOPUS:85091612039
SN - 1001-0602
VL - 31
SP - 141
EP - 156
JO - Cell Research
JF - Cell Research
IS - 2
ER -
Xu F, Du W, Zou Q, Wang Y, Zhang X, Xing X et al. COPII mitigates ER stress by promoting formation of ER whorls. Cell Research. 2021 Feb;31(2):141-156. doi: 10.1038/s41422-020-00416-2