Please report any queries concerning the funding data grouped in the sections named "Externally Awarded" or "Internally Disbursed" (shown on the profile page) to
your Research Finance Administrator. Your can find your Research Finance Administrator at https://www.ucl.ac.uk/finance/research/rs-contacts.php by entering your department
Please report any queries concerning the student data shown on the profile page to:
Email: portico-services@ucl.ac.uk
Help Desk: http://www.ucl.ac.uk/ras/portico/helpdesk
Email: portico-services@ucl.ac.uk
Help Desk: http://www.ucl.ac.uk/ras/portico/helpdesk
Publication Detail
Genetic screen identifies non-mitochondrial proteins involved in the maintenance of mitochondrial homeostasis
-
Publication Type:Journal article
-
Authors:Rolland S, Conradt B
-
Publication date:2022
-
Journal:microPublication Biology
-
Status:Published
-
Country:United States
-
Print ISSN:2578-9430
-
Language:English
-
Publisher URL:
-
Notes:© 2022 by the authors. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International (CC BY 4.0) License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
The mitochondrial unfolded protein response (UPR mt ) is an important stress response that ensures the maintenance of mitochondrial homeostasis in response to various types of cellular stress. We previously described a genetic screen for Caenorhabditis elegans genes, which when inactivated cause UPR mt activation, and reported genes identified that encode mitochondrial proteins. We now report additional genes identified in the screen. Importantly, these include genes that encode non-mitochondrial proteins involved in processes such as the control of gene expression, post-translational modifications, cell signaling and cellular trafficking. Interestingly, we identified several genes that have been proposed to participate in the transfer of lipids between peroxisomes, ER and mitochondria, suggesting that lipid transfer between these organelles is essential for mitochondrial homeostasis. In conclusion, this study shows that the maintenance of mitochondrial homeostasis is not only dependent on mitochondrial processes but also relies on non-mitochondrial processes and pathways. Our results reinforce the notion that mitochondrial function and cellular function are intimately connected.
› More search options
UCL Researchers