A mitochondrial-associated link between an effector caspase and autophagic flux
Year: 2014
Type: editorial
Abstract: It has become evident that caspases function in nonapoptotic cellular processes in addition to the canonical role for caspases in apoptotic cell death. We recently demonstrated that the Drosophila effector caspase Dcp-1 localizes to the mitochondria and positively regulates starvation-induced autophagic flux during mid-oogenesis. Loss of Dcp-1 leads to elongation of the mitochondrial network, increased levels of the adenine nucleotide translocase sesB, increased ATP levels, and a reduction in autophagy. We found that sesB is a negative regulator of autophagic flux, and Dcp-1 interacts with sesB in a nonproteolytic manner to regulate its stability, uncovering a novel mechanism of mitochondrial associated, caspase-mediated regulation of autophagy in vivo.
Source: Autophagy
DOI: 10.4161/auto.32170
Authors: Lindsay DeVorkin, Sharon M Gorski
Institutions: BC Cancer Agency, Simon Fraser University
Language: English
Subfield: Cell Biology
Domain: Life Sciences
Open Access status: hybrid
Award: G109972196
OpenAlex ID: W2091385166
