Repository logo
 

The mitochondria–endoplasmic reticulum contact sites: a signalling platform for cell death

Accepted version
Peer-reviewed

Type

Article

Change log

Authors

McBride, HM 

Abstract

Mitochondria evolved as an endosymbiont providing the cell with a dizzying array of catabolic and anabolic processes essential for life. However, mitochondria have retained the ability to kill from within, and are widely considered the final executioners of programmed cell death. The groundbreaking discovery over 25 years ago that mitochondrial cytochrome c is released into the cytosol shone new and unexpected light onto this old organelle, revitalizing the field. The Bcl-2 family of proteins plays a central role in the maintenance of mitochondrial membrane integrity, but other factors are also involved in the cell death program. Indeed, contacts with the endoplasmic reticulum (ER), mitochondrial division and inner membrane cristae remodeling have emerged as key regulators of cytochrome c release. This review will focus on recent progress to define the functional contribution of the apoptotic ER/mitochondrial interface, which couples mitochondrial fission and cristae remodeling to calcium and lipid fluxes.

Description

Keywords

Animals, Apoptosis, Calcium, Cytosol, Endoplasmic Reticulum, Humans, Mitochondria, Mitochondrial Dynamics, Mitochondrial Membranes

Journal Title

Current Opinion in Cell Biology

Conference Name

Journal ISSN

0955-0674
1879-0410

Volume Title

47

Publisher

Elsevier
Sponsorship
Medical Research Council (MC_UU_00015/7)
Studies in this area were funded by Canadian Institutes of Health Research (CIHR) (PT-71405) and Canadian Cancer Society Research Institute (CCSRI) (#704826) to HMM, and Medical Research Council, UK (MC_UP_1601/1) to JP. HMM was supported by a Canada Research Chair Tier 1.