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J Cell Sci. 2018 Jan 4;131(1). pii: jcs208686. doi: 10.1242/jcs.208686.

A novel fluorescent reporter detects plastic remodeling of mitochondria-ER contact sites.

Author information

1
Life Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China.
2
Life Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China ctong@zju.edu.cn.

Abstract

Mitochondria-ER contact sites (MERCs) enable communication between the ER and mitochondria and serve as platforms for many cellular events, including autophagy. Nonetheless, the molecular organization of MERCs is not known, and there is no bona fide marker of these contact sites in mammalian cells. In this study, we designed a genetically encoded reporter using split GFP protein for labeling MERCs. We subsequently analyzed its distribution and dynamics during the cell cycle and under stressful cellular conditions such as starvation, apoptosis and ER stress. We found that MERCs are dynamic structures that undergo remodeling within minutes. Mitochondrial morphology, but not ER morphology, affected the distribution of MERCs. We also found that carbonyl cyanidem-chlorophenyl hydrazone (CCCP) and oligomycin A treatment enhanced MERC formation. The stimulations that led to apoptosis or autophagy increased the MERC signal. By contrast, increasing cellular lipid droplet load did not change the pattern of MERCs.

KEYWORDS:

Autophagy; Endoplasmic reticulum; Mitochondria; Mitochondria–ER contacts; Split GFP

PMID:
29158224
DOI:
10.1242/jcs.208686
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Conflict of interest statement

Competing interestsThe authors declare no competing or financial interests.

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