| Literature DB >> 26926495 |
Amit S Joshi1, Naomi Fei1, Miriam L Greenberg2.
Abstract
Cardiolipin (CL) is the signature phospholipid of mitochondrial membranes. CL deficiency leads to defects in mitochondrial function. Using a targeted synthetic lethality screen to identify defects that exacerbate CL deficiency, we determined that deletion of mitochondrial morphology genes in cells lacking CL leads to severe growth defects. We show that ER membrane proteins Get1p and Get2p are required for maintaining normal levels of CL. We propose that these proteins regulate the level of CL by maintaining wild type-like tubular mitochondrial morphology. The genetic interactions observed in this study identify novel physiological modifiers that are required for maintenance of CL levels and mitochondrial morphology. © FEMS 2016. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.Entities:
Keywords: Barth syndrome; cardiolipin; mitochondria morphology
Mesh:
Substances:
Year: 2016 PMID: 26926495 PMCID: PMC5731434 DOI: 10.1093/femsyr/fow019
Source DB: PubMed Journal: FEMS Yeast Res ISSN: 1567-1356 Impact factor: 2.796