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. 2020 May 27;21(11):3781. doi: 10.3390/ijms21113781

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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(A) Membrane contact site (MCS) formation by MITOL-MFN2 axis. MITOL ubiquitinates mitochondrial MFN2. The ubiquitinated MFN2 enhances its GTPase activity, triggering trans-oligomerization between mitochondrial MFN2 and ER-localized MFN2 for tethering both organelles; mitochondria and the ER; (B) UPR regulation by MITOL-IRE1α axis. MITOL ubiquitinates IRE1α at ER-mitochondria contact site in unstressed and low-stressed conditions regarding the ER. The ubiquitination of IRE1α does not perturbate the oligomerization itself in response to ER stress, however, leading to short-term stabilization and smaller oligomerization. In contract, the ubiquitination by MITOL is reduced under severe or chronic ER stress, resulting in continuous oligomerization of IRE1α and apoptotic switching of IRE1α signaling.